BlueCross and BlueShield of Montana Medical Policy/Codes
Kinesin-like protein 6 (KIF6) Genotyping for Predicting Cardiovascular Risk and/or Effectiveness of Statin Therapy
Chapter: Genetic Testing
Current Effective Date: July 18, 2013
Original Effective Date: October 13, 2011
Publish Date: July 18, 2013
Revised Dates: April 6, 2012; April 10, 2013

Genetic testing to determine the KIF6 Trp719Arg variant status of patients is being evaluated as a prognostic test to predict risk of future cardiovascular events and/or as a pharmacogenetic test to predict response to statin therapy, particularly in high-risk patients.

Analysis of prospective observational studies of cardiovascular health and of the placebo arm of randomized controlled trials (RCTs) of statin intervention in at-risk populations has suggested a significant association between the Trp719Arg single nucleotide polymorphism (SNP; rs20455) in kinesin-like protein 6 (KIF6) and the development of clinical coronary artery disease (CAD). Approximately 60% of the population carries the putative KIF6 high-risk 719Arg allele. Moreover, carriers of the 719Arg allele in the treatment arms of the statin trials appeared to be at no increased risk, or at decreased risk, of CAD or recurrent myocardial infarction (MI), depending on the intensity of the statin therapy. These results supported the development of a KIF6 Trp719Arg genotyping test for use as a predictor of CAD risk and of the likely effectiveness of statin therapy.

Celera Corporation, now a wholly owned subsidiary of Quest Diagnostics, Inc., holds a U.S. patent relating to methods of determining heart attack risk by detecting the KIF6 gene variant and reduction of such increased risk by statin therapy. Celera's Berkeley HeartLab (BHL) subsidiary has been offering KIF6 genotyping (KIF6-StatinCheck™ Genotype Test) since July 2008. San Francisco General Hospital’s Clinical Chemistry Laboratory (University of California, San Francisco), is the only non-Celera lab to obtain a license to develop a KIF6 LTD; a small number of clinical labs/health care groups have negotiated with Celera to offer the test by sending it to BHL (e.g., Aurora Health Care of Milwaukee, WI).

Regulatory Status

The KIF6 genotyping test is not a manufactured test kit and has not been reviewed by the Food and Drug Administration (FDA) . Rather, it is a laboratory-developed test (LDT), offered by clinical laboratories licensed under Clinical Laboratory Improvement Amendments (CLIA) for high-complexity testing. The company submitted a Premarket Approval application to the U.S. Food and Drug Administration in January, 2011, for their KIF6 Genotyping Assay performed on Abbott's m2000™ instrument system. However, on April 7, 2011 the FDA sent a letter to Celera indicating that its application is not approvable “without major amendment.” The data and publications submitted were deemed “insufficient to demonstrate the safety and effectiveness of the device for its proposed intended use.” The agency indicated that additional data on clinical utility may be required, which could include conducting a randomized controlled clinical trial.



Blue Cross Blue Shield of Montana (BCBSMT) considers kinesin-like protein 6 (KIF6) genotyping experimental, investigational and unproven for predicting cardiovascular risk and/or the effectiveness of statin therapy.

Federal Mandate

Federal mandate prohibits denial of any drug, device or biological product fully approved by the FDA as investigational for the Federal Employee Program (FEP). In these instances coverage of these FDA-approved technologies are reviewed on the basis of medical necessity alone.

Rationale for Benefit Administration
This medical policy was developed through consideration of peer reviewed medical literature, FDA approval status, accepted standards of medical practice in Montana, Technology Evaluation Center evaluations, and the concept of medical necessity. BCBSMT reserves the right to make exceptions to policy that benefit the member when advances in technology or new medical information become available.

The purpose of medical policy is to guide coverage decisions and is not intended to influence treatment decisions. Providers are expected to make treatment decisions based on their medical judgment. Blue Cross and Blue Shield of Montana recognizes the rapidly changing nature of technological development and welcomes provider feedback on all medical policies.

When using this policy to determine whether a service, supply or device will be covered please note that member contract language will take precedence over medical policy when there is a conflict.

Literature Review

The kinesin-like protein 6 (KIF6) belongs to the kinesin superfamily of proteins involved in intracellular transport. The exact function of the KIF6 gene product is as yet undetermined. According to one article, the gene is not expressed in the vasculature, the primary site of atherosclerosis. Rather, it is expressed in low levels in the brain, connective tissue, colon, eye, pharynx, skin, and testes. (1) In contrast, a study presented at the American Heart Association, Arteriosclerosis, Thrombosis and Vascular Biology 2010 Scientific Sessions, reported data derived from tissue immunohistochemistry, locating KIF6 protein in macrophages surrounding neovessels and in foam cells in human atherosclerotic lesions. (2) Nevertheless, there is as yet no strong evidence that KIF6 protein plays a biological role in atherosclerosis, lipid metabolism, coronary artery disease (CAD), or myocardial infarction (MI).

Clinical validity

The Trp719Arg SNP in the KIF6 gene was deliberately investigated and associated with CAD outcomes in retrospective evaluations of prospective, observational studies (Table, Part 1), (3-5) and in retrospective evaluations of the placebo arms of randomized, controlled trials (RCTs) of statin therapy (Table, Part 2). (6, 7) Whether the initial inclusion of KIF6 markers in early studies initiated by Celera was based on candidate gene selection or on larger, gene-scanning studies is unclear from the published literature, and claims of critics and test developers on this point are contradictory.

In both relatively unselected prevention cohorts (Table, Part 1), and in trial populations selected for high risk of a CHD event, the Trp719Arg SNP is significantly associated with CHD outcomes at hazard ratios (HR) in the range of approximately 1.1 to 1.5.

In the statin treatment arms of RCTs, carriers of the 719Arg variant were at decreased risk of an event compared to controls, whereas non-carriers appeared to derive little if any benefit from statin treatment. In the analysis of the Pravastatin or Atorvastatin Evaluation and Infection Therapy: Thrombolysis in Myocardial Infarction 22 trial, which compared less intensive (pravastatin) versus more intensive (atorvastatin) therapy, carriers of the 719Arg variant received significantly greater benefit from intensive therapy than non-carriers. (8)

However, a large meta-analysis of 19 case-control studies (Table, Part 3) (9) found no association between the Trp719Arg SNP and CAD, even when the overall population was restricted to Europeans with early onset disease (less likely to be confounded by statin therapy), to Europeans with MI, or to Europeans with early onset MI. The authors of the meta-analysis note that they examined only non-fatal MI; if the Trp719Arg variant increases the risk of fatal CAD more than the risk of non-fatal CAD, the study results could be biased toward the null. The meta-analysis could not examine whether the effect on risk was modified by statin therapy.

In addition to the findings of the meta-analysis, none of the several, large genome-wide association studies for CAD or MI reported any SNPs at the KIF6 locus as significant. (10-14) For this reason, some have considered the possible candidate (i.e., pre-selected) gene approach to the KIF6 variant analysis by the test developers as potentially flawed, given the current lack of biologic plausibility.

The most recently published evidence (Table, Part 4) is consistent with the meta-analysis results. Ridker et al. (15) evaluated the effect of the KIF6 variant on the outcomes of 8,781 Caucasian trial participants in the JUPITER (Justification for Use of Statins in Primary Prevention, An Intervention Trial Evaluating Rosuvastatin) study and in the trial as a whole. Rosuvastatin was equally effective at reducing cardiovascular event rates among carriers and non-carriers of the KIF6 variant; results for trial participants as a whole were essentially identical. Hopewell et al. (16) evaluated data from the Heart Protection Study on more than 18,000 patients with prior cardiovascular disease or high predisposing risk and compared outcomes after treatment with simvastatin or placebo. The authors reported no association of KIF6 variant status with outcome in the placebo arm, nor in the treatment arm; simvastatin reduced the incidence of coronary events equally regardless of KIF6 status. Hoffmann et al. (17) evaluated a narrowly focused population of patients with type 2 diabetes and less than two years previous treatment by hemodialysis, randomly assigned to double-blinded treatment with either 20mg of atorvastatin (n = 619) or placebo (n = 636). In neither the placebo nor the statin group was there any association of KIF6 genotype with major cardiovascular events. This study was limited because statins did not achieve the expected improvement in survival despite significantly decreasing low-density lipoprotein (LDL) cholesterol. Nevertheless, taken together, these three studies show that in different populations with different levels of vascular risk and treated with different statin drugs, there was no measureable effect of the KIF6 variant on statin response, nor any association with vascular risk.

Another recent study, by Arsenault et al. (18) investigated whether carriers of the KIF6 variant obtain more benefit from high-dose statin therapy than do non-carriers by retrospective analysis of two prospective trials. In the Treating to New Targets (TNT) study, 4,599 patients with stable coronary heart disease and LDL cholesterol levels <130 mg/dL, randomly assigned to receive either 10 or 80 mg of atorvastatin per day and followed up for a median of 4.9 years, were genotyped. KIF6 genotype did not affect risk for future events within treatment arms. Genotype subgroups had a similar benefit from 80 mg atorvastatin compared to 10 mg except for the homozygous variant subgroup, which was the only group with a statistically significant benefit from the higher statin dose, but interaction for genotype by treatment was not significant. The Incremental Decrease in End Points Through Aggressive Lipid-Lowering (IDEAL) study enrolled patients with a history of MI and randomized them to high-dose atorvastatin or usual dose simvastatin and followed for a median of 4.8 years. Of the 8,888 enrolled, 6,541 were genotyped; there were no significant differences by KIF6 genotype in comparative response to statin treatment, and the interaction for genotype by treatment was not significant.

Clinical utility

Based on the earlier retrospective analyses of statin trials, and the apparent association of the Trp719Arg variant with treatment benefit, genotyping was recommended to predict which patients would most benefit from pravastatin or atorvastatin treatment. For carriers of the KIF6 variant, the number needed to treat (NNT) to prevent one event is approximately 10 to 20, whereas for non-carriers the NNT is approximately 80 to more than 100. (19) Thus, it has been suggested that for patients at clinically high risk who are non-carriers, additional intervention may be appropriate; for variant carriers at clinically lower risk who might not normally be treated, statin treatment may provide greater than average benefit. However, these management changes have not been tested prospectively. The more recent retrospective evaluations of prospective, randomized trials (Table, part 4), conducted in large patient populations, indicate that non-carriers of the KIF6 variant benefit from statin therapy to the same degree as variant carriers, likely invalidating the rationale for genotyping and basing statin treatment recommendations on the test result. (20)

Celera has been working with pharmacy benefit manager Medco to generate real-world evidence regarding patient knowledge of KIF6 genotype status and statin compliance. A prospective study has already completed enrollment (NCT01068834; Additional KIF6 Risk Offers Better Adherence to Statins, or AKROBATS, trial) and will compare statin adherence in those who learn about their carrier status versus those who do not. Preliminary data were reported at the 2011 American Society of Human Genetics annual meeting; the authors indicated that patients taking statins were more likely to take their medications if they had been tested for the KIF6 variant. Conclusions await completion of the trial and full publication.

Table. Results of individual studies investigating differential effects of KIF6 genotype on cardiovascular outcomes and Meta-analysis of the association of KIF6 with CAD outcomes.



Patients Evaluated


KIF6 Association Evaluated


Results: Observational Study or Placebo Arm, KIF6V carriers vs. non-carriers

Results: Statin Arm vs. Placebo Arm (unless otherwise stated)

Part 1 KIF6 variant association with CAD outcomes in retrospective evaluations of prospective, observational studies

Morrison et al. 2007 Retrospective evaluation of ARIC study (3)  

U.S. individuals aged 45–64 years  

MI, CHD death, or coronary revascularization

HR: 1.09
(95% CI,1.00-1.19) 


Shiffman et al., 2008
Retrospective evaluation of CHS (5)  

Adults aged 65 years and older  

Incident MI 

HR: 1.29
(90% CI, 1.1-1.52)* (95% CI, 1.06-1.6)**  


Shiffman et al., 2008
Retrospective evaluation of
WHS (4)  

Healthy Caucasian American women  

Incident CHD event (MI, coronary revascularization, or CV-related death) or incident ischemic stroke  

CHD HR: 1.24
(95% CI, 1.04-1.46)
MI HR: 1.34
(95% CI, 1.02-1.75)
Stroke HR: not sig.


Part 2 KIF6 variant association with CAD outcomes in retrospective evaluations of randomized, controlled trials of statin therapy

Lakoubova et al., 2008
Retrospective evaluation of
CARE study (7)  

Caucasian MI survivors with total cholesterol <240 mg/dL  

Recurrent fatal or non-fatal MI  

HR: 1.50
(95% CI, 1.05-2.15)  

Among KIF6V carriers: HR: 0.63 (0.46–0.87) Among non-carriers: HR: 0.80 (0.52–1.24)  

Shiffman et al., 2010
Retrospective evaluation of
CARE study (21)  

MI survivors (all ethnicities) with total cholesterol <240 mg/dL  

Recurrent fatal or non-fatal MI  


Adjusted for self-reported ethnicity,
Among KIF6V carriers:
HR: 0.63 (0.49-0.83)
Among non-carriers:
HR: 1.01 (0.69-1.45)  

Lakoubova et al., 2008
Nested case-control study from
WOSCOPS trial (7)  

Men with hyper-cholesterolemia but no history of MI  

Nonfatal MI, revascularization procedures, or death from CHD  

OR: 1.55
(95% CI, 1.14-2.09)  

Among KIF6V carriers: HR: 0.50 (0.38–0.68) Among non-carriers: HR: 0.91 (0.64–1.28)  

Iakoubova et al., 2008
Retrospective evaluation of
PROVE IT-TIMI 22 (8)  

Patients hospitalized for MI or high-risk unstable angina  

Composite endpoint: all-cause mortality, MI, unstable angina, or stroke  

(no placebo arm)  

Intensive vs. moderate statin therapy arms among:
KIF6V carriers
HR: 0.59 (0.45-0.77),
Non-KIF6V carriers
HR: 0.94 (0.70-1.27)  

Iakoubova et al., 2010
Retrospective evaluation of
PROSPER study (6)

Older patients with preexisting vascular disease  

Composite endpoint: death from CHD, nonfatal MI, or fatal/ nonfatal stroke


HR: 1.28
(95% CI, 0.98-1.69)  

Among KIF6V carriers:
HR: 0.66 (0.52-0.86)
Among non-carriers:
HR: 0.94 (0.69-1.28)  


Older patients at increased risk for vascular disease  



No benefit 

Part 3 Meta-analysis of KIF6 variant association with CAD outcomes

Assimes et al., 2010
Meta-analysis of 19 case-control studies(9)

17,000 cases,
39,369 controls 

CAD cases with and without a
diagnosis of non-fatal MI  

OR: 0.98
(95% CI, 0.95-1.02)  



Europeans, subgroup with very early onset disease

(as above) 

OR: 0.99
(95% CI, 0.94-1.04)  



Europeans, restricting cases to MI  

(as above) 

OR: 0.99
(95% CI, 0.96-1.03)  



Europeans, restricting cases to early onset MI  

(as above) 

OR: 1.03
(95% CI, 0.98-1.09)  


Part 4 Recent publications

Ridker et al., 2011 Retrospective evaluation of prospective JUPITER study (15) Rosuvastatin vs. placebo  

Men and women free of diabetes or prior cardiovascular disease  

Composite: CV death, nonfatal MI, nonfatal stroke, hospitalization for unstable angina, or arterial revascularization,

(95% CI, 0.66-1.26) 

Among KIF6V carriers: HR:0.61 (0.43-0.87) Among non-carriers: HR:0.59 (0.39-0.88) P-interact=0.90  

Hopewell et al., 2011 Retrospective evaluation of prospective Heart Protection Study (16) Simvastatin vs. placebo

Individuals at high risk for or a previous diagnosis of CV disease  

Composite: CHD death, nonfatal MI, strokes, coronary or noncoronary revascularizations  

No significant effect on risk of major CV events, regardless of modeling approach (p= 0.54 to 0.76)  

Among KIF6V carriers: 23% (16% - 29%) Among non-carriers: 24% (17% - 31%) P-interact=0.4 to 0.7  

Hoffmann et al., 2011 Retrospective evaluation of 4D prospective study (17) Atorvastatin vs. placebo  

Patients with T2DM and <2 year prior hemodialysis treatment 

Composite: death from cardiac causes, MI, or stroke  

(95% CI, 0.66–1.05) 

Among statin-treated, KIF6V carriers vs. non-carriers: HR=0.96 (0.76–1.23)  

Arsenault et al. 2011 Retrospective evaluation of prospective TNT (80 vs. 10 mg/day atorvastatin) and IDEAL (80mg/day atorvastatin vs. 20-40 mg/day simvastatin) studies (18)


TNT: patients with stable CHD and LDL-C levels<130 mg/dL  






IDEAL: patients with a history of MI  

Composite: coronary death, nonfatal MI, resuscitation after cardiac arrest and fatal or nonfatal stroke



Among KIF6V carriers: 0.85 (0.66-1.11) Among homozygote carriers: 0.44 (0.23-0.84) Among non-carriers: 0.81 (0.59-1.11) P-interact=0.81  


Among KIF6V carriers: 0.91 (0.58-1.43) Among homozygote carriers: 0.88 (0.62-1.07) Among non-carriers: 0.85 (0.67-1.10), P-interact=0.91  

Abbreviations: CAD, coronary artery disease; CHD, coronary heart disease; CV, cardiovascular; MI, myocardial infarction; T2DM, type 2 diabetes mellitus; OR, odds ratio; HR, hazard ratio; CI, confidence interval; N/A, not applicable; MI, myocardial infarction; ARIC, Atherosclerosis Risk in Communities cohort; CHS, Cardiovascular Health Study; CARE, Cholesterol and Recurrent Events trial; WOSCOPS, West of Scotland Coronary Prevention Study; PROVE IT-TIMI 22, Pravastatin or Atorvastatin Evaluation and Infection Therapy: Thrombolysis in Myocardial Infarction 22 trial; WHS, Women's Health Study; PROSPER, PROspective Study of Pravastatin in the Elderly at Risk; JUPITER, Justification for Use of Statins in Primary Prevention, An Intervention Trial Evaluating Rosuvastatin; TNT, Treating to New Targets; IDEAL, Incremental Decrease in End Points Through Aggressive Lipid-Lowering.


**Calculated from published data. 

Practice Guidelines and Position Statements

No reference to KIF6 was found in the 2010 American College of Cardiology Foundation/American Heart Association Practice Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults. (22)

Hayes, Inc./Hayes Genetic Test Evaluation team conducted an assessment of “KIF6 p.Trp719Arg Testing to Assess Risk of Coronary Artery Disease and/or Statin Response” and concluded that the evidence was insufficient to determine utility, due largely to lack of evidence supporting clinical utility.(23)

Ongoing Clinical Trials

The Additional KIF6 Risk Offers Better Adherence to Statins (AKROBATS) trial ( Identifier: NCT01068834) is sponsored by Medco Health Solutions, Inc. in collaboration with Celera and is currently enrolling patients by invitation only. The purpose of this study is to determine whether providing subjects their KIF6 carrier status (and associated cardiovascular event risk) will improve adherence to statin medications.

Funded under American Recovery and Reinvestment Act of 2009 (ARRA) Investments in Coronary Artery Disease, Brigham and Women’s Hospital is conducting the Genetic Risk Stratification to Identify Individuals for Early Statin Therapy study (Project No. 1RC1HL099634-01). Goals of the study are to 1) test whether specific panels of genetic variants identify patients who experience a greater clinical benefit with statin therapy using retrospective data; and 2) test whether specific panels of genetic variants identify patients who experience a higher risk of statin-induced adverse effects in the same cohorts.


The data supporting the association of the KIF6 Trp719Arg SNP with CAD outcomes are contradictory. The most recent evidence from large populations at different levels of vascular risk does not support a significant association with future CAD outcomes. Moreover, the biologic function of the KIF6 protein is currently unknown. Thus, the clinical validity for the KIF6 genotyping test has not been shown. The most recent results of treatment trials indicate that the efficacy of statin treatment appears to be similar in carriers and non-carriers of the mutation. It has not been determined whether the results of the test can be used to improve patient management decisions and improve outcomes. Thus, testing for KIF6 status to determine statin treatment benefit is considered experimental, investigational and unproven.


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Procedure and diagnosis codes on Medical Policy documents are included only as a general reference tool for each policy. They may not be all-inclusive.           

The presence or absence of procedure, service, supply, device or diagnosis codes in a Medical Policy document has no relevance for determination of benefit coverage for members or reimbursement for providers. Only the written coverage position in a medical policy should be used for such determinations.           

Benefit coverage determinations based on written Medical Policy coverage positions must include review of the member’s benefit contract or Summary Plan Description (SPD) for defined coverage vs. non-coverage, benefit exclusions, and benefit limitations such as dollar or duration caps. 

Rationale for Benefit Administration
ICD-9 Codes

Experimental, investigational and unproven for all diagnoses.

ICD-10 Codes

Experimental, investigational and unproven for all diagnoses.

Procedural Codes: 84999
  1. Marian AJ. Surprises of the genome and "personalized" medicine. J Am Coll Cardiol 2008; 51(4):456-8.
  2. Rosenfeld ME, Preusch M, Shiffman D et al. KIF6, an Emerging Coronary Heart Disease Risk Marker Expressed by Macrophages in Atherosclerotic Lesions in Humans and Mice. American Heart Association Arteriosclerosis, Thrombosis and Vascular Biology Scientific Sessions 2010; P692.
  3. Morrison AC, Bare LA, Chambless LE et al. Prediction of coronary heart disease risk using a genetic risk score: the Atherosclerosis Risk in Communities Study. Am J Epidemiol 2007; 166(1):28-35.
  4. Shiffman D, Chasman DI, Zee RY et al. A kinesin family member 6 variant is associated with coronary heart disease in the Women's Health Study. J Am Coll Cardiol 2008; 51(4):444-8.
  5. Shiffman D, O'Meara ES, Bare LA et al. Association of gene variants with incident myocardial infarction in the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol 2008; 28(1):173-9.
  6. Iakoubova OA, Robertson M, Tong CH et al. KIF6 Trp719Arg polymorphism and the effect of statin therapy in elderly patients: results from the PROSPER study. Eur J Cardiovasc Prev Rehabil 2010; 17(4):455-61.
  7. Iakoubova OA, Tong CH, Rowland CM et al. Association of the Trp719Arg polymorphism in kinesin-like protein 6 with myocardial infarction and coronary heart disease in 2 prospective trials: the CARE and WOSCOPS trials. J Am Coll Cardiol 2008; 51(4):435-43.
  8. Iakoubova OA, Sabatine MS, Rowland CM et al. Polymorphism in KIF6 gene and benefit from statins after acute coronary syndromes: results from the PROVE IT-TIMI 22 study. J Am Coll Cardiol 2008; 51(4):449-55.
  9. Assimes TL, Holm H, Kathiresan S et al. Lack of association between the Trp719Arg polymorphism in kinesin-like protein-6 and coronary artery disease in 19 case-control studies. J Am Coll Cardiol 2010; 56(19):1552-63.
  10. Samani NJ, Erdmann J, Hall AS et al. Genomewide association analysis of coronary artery disease. N Engl J Med 2007; 357(5):443-53.
  11. Kathiresan S, Voight BF, Purcell S et al. Genome-wide association of early-onset myocardial infarction with single nucleotide polymorphisms and copy number variants. Nat Genet 2009; 41(3):334-41.
  12. McPherson R, Pertsemlidis A, Kavaslar N et al. A common allele on chromosome 9 associated with coronary heart disease. Science 2007; 316(5830):1488-91.
  13. Helgadottir A, Thorleifsson G, Manolescu A et al. A common variant on chromosome 9p21 affects the risk of myocardial infarction. Science 2007; 316(5830):1491-3.
  14. Wellcome Trust Case Control Consortium. Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 2007; 447(7145):661-78.
  15. Ridker PM, MacFadyen JG, Glynn RJ et al. Kinesin-like protein 6 (KIF6) polymorphism and the efficacy of rosuvastatin in primary prevention. Circ Cardiovasc Genet 2011; 4(3):312-7.
  16. Hopewell JC, Parish S, Clarke R et al. No impact of KIF6 genotype on vascular risk and statin response among 18,348 randomized patients in the heart protection study. J Am Coll Cardiol 2011; 57(20):2000-7.
  17. Hoffmann MM, Marz W, Genser B et al. Lack of association between the Trp719Arg polymorphism in kinesin-like protein-6 and cardiovascular risk and efficacy of atorvastatin among subjects with diabetes on dialysis: the 4D study. Atherosclerosis 2011; 219(2):659-62.
  18. Arsenault BJ, Boekholdt SM, Hovingh GK et al. The 719Arg Variant of KIF6 and Cardiovascular Outcomes in Statin-Treated, Stable Coronary Patients of the TNT and IDEAL Prospective Studies. Circ Cardiovasc Genet 2011 [Epub ahead of print].
  19. Li Y, Iakoubova OA, Shiffman D et al. KIF6 polymorphism as a predictor of risk of coronary events and of clinical event reduction by statin therapy. Am J Cardiol 2010; 106(7):994-8.
  20. Musunuru K. Lack of association of KIF6 genotype with vascular disease and statin response. Circ. Cardiovasc Genet 2011; 4(4):467-8.
  21. Shiffman D, Sabatine MS, Louie JZ et al. Effect of pravastatin therapy on coronary events in carriers of the KIF6 719Arg allele from the cholesterol and recurrent events trial. Am J Cardiol 2010; 105(9):1300-5.
  22. Greenland P, Alpert JS, Beller GA et al. 2010 ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2010; 122(25):e584-636.
  23. Allingham-Hawkins D, Lea A, Levine S. KIF6 p.Trp719Arg testing to assess risk of coronary artery disease and/or statin response. PLoS Curr 2010; 2:RRN1191
  24. KIF6 Genotyping for Predicting Cardiovascular Risk and/or Effectiveness of Statin Therapy. Chicago, Illinois: Blue Cross Blue Shield Association Medical Policy Reference Manual (2012 February) Medicine 2.04.67.
October 2011 New Policy: no specific CPT genetic testing codes for this policy
April 2012 Policy updated with literature review, references 15-24 added. No change to policy statement.
April 2013 Policy formatting and language revised.  Policy statement unchanged.  Title changed from "KIF6 Genotyping for Predicting Cardiovascular Risk and/or Effectiveness of Statin Therapy" to "Kinesin-like protein 6 (KIF6) Genotyping for Predicting Cardiovascular Risk and/or Effectiveness of Statin Therapy".  Removed codes 83890, 83891, 83892, 83893, 83894, 83896, 83897, 83898, 83900, 83901, 83902, 83903, 83904, 83905, 83906, 83907, 83908, 83909, 83912.
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Kinesin-like protein 6 (KIF6) Genotyping for Predicting Cardiovascular Risk and/or Effectiveness of Statin Therapy