Given the observation that ASMaseMyh6KO mice are protected from experimental cardiomyopathy and demonstrated in cellular experiments that ASMase was responsive to cardiac hypertrophy through NADPH oxidases activations and apoptosis, we hypothesized that the protective effects of ASMase deficiency were attributed to blockade of oxidative stress and apoptosis mediated by NAPDH oxidases. Here, FMO5 is linked to cardiomyopathy.