Interestingly overexpression of iNOS specifically in cardiomyocytes of transgenic mice results in cardiac hypertrophy and sudden cardiac death (Mungrue et al., 2002), whilst energetic depletion as a result of pathogenic cardiomyopathy mutations results in increased the generation of reactive oxygen species by the mitochondria (Ashrafian et al., 2003; Sacchetto et al., 2019). Here, NOS2 is linked to cardiomyopathy.