suggest that a genetic risk by environmental interaction might account for such inconsistency because the targeted genetic effects are most strongly expressed in environments that provide little support for cessation (e.g., no effective pharmacotherapy). None of the previous studies has reported this interaction, which could potentially explain the apparently inconsistent results in this area. Such interactions between genetic variants and treatment can serve as the basis for personalized medicine. The TAG consortium examined a different cessation phenotype (former vs. current smoker) and reported a modest association with CHRNA5-CHRNA3-CHRNB4 (p <1*10−4) (10).
