Moreover, depletion of inducible nitric oxide synthase (iNOS) in an experimental study of wild-type mice with chronic transverse aortic constriction beneficially affect cardiac hypertrophy, dilation, fibrosis, and dysfunction, implying the detrimental effects of iNOS dysregulation in the maladaptive response to systolic overload of the heart [96]. This evidence concerns the gene NOS2 and cardiac hypertrophy.