The insertion/deletion (I/D) polymorphism in the ACE gene has been implicated in increased cardiovascular risk by modulating angiotensin II levels, thereby influencing vascular function, inflammation, and thrombosis.[3,4] Several studies have reported a strong association between the ACE D allele and the development of CAD, particularly in populations with high genetic homogeneity.[5]. The gene discussed is ACE; the disease is coronary artery disorder.