While smoking may appear to decrease the risk of myocardial infarction by induction of the homozygous allele, smokers with the CYP1A2*1A allele do not necessarily bode better than slow metabolizers because smoking is an established independent cardiovascular disease risk factor with other pathologic mechanisms beyond the protective effects of CYP1A2 on caffeine regulation.27 The gene discussed is CYP1A2; the disease is cardiovascular disorder.