By taking advantage of the genetic variability of ADIPOQ gene described in recent genome-wide association studies,24,36 we observed that genetically determined reduction of adiponectin levels is also associated with increased NADPH-stimulated O2− in the heart of patients with IHD (an association independent of other covariates, including BNP), implying that low adiponectin production in the human AT is causally associated with higher myocardial NADPH oxidase activity. This evidence concerns the gene FMO5 and myocardial ischemia.