Given the role of eNOS and the KATP channel in the fine regulation of CBF, as well as the evidence of the potential primary role of genetic susceptibility in IHD, we hypothesize that SNPs of the NOS3 and KCNJ11 genes may potentiate the interaction between eNOS and the KATP channel, exploiting an evident effect on CBF regulation and a subsequent hemodynamic effect, influencing the predisposition to IHD. The gene discussed is CEBPZ; the disease is myocardial ischemia.