Many authors have explained this inconsistency by the fact that the CYP2C19 effect size on Clopidogrel effectiveness may parallel the effect of this molecule for a given clinical indication; high in patients at high risk for recurrent CVD events in the absence of adequate anti platelet therapy (e.g., ACS/PCI), and low or non-existent for clinical situations where the drug has reduced effect on cardiovascular outcomes (e.g., stable angina, atrial fibrillation and peripheral vascular disease) [27–34]. The gene discussed is CYP2C19; the disease is angina pectoris.