In particular, Khan et al. have shown that nNOS and XOR are colocalized in the SR of murine cardiomyocytes and that absence or inhibition of nNOS is associated with an increased XOR-dependent superoxide generation, suggesting the possibility that the cardiac phenotype of nNOS−/− mice, characterized by the presence of ventricular hypertrophy, may be a consequence of increased myocardial oxidative stress [42]. This evidence concerns the gene NOS1 and Ventricular hypertrophy.