Genetic and epidemiological studies indicate that deficiencies in NO synthesis and bioavailability derived from eNOS are central to the pathogenesis of hypertension, reduced cardiac and endothelial cell function, and metabolic disorders (Emdin et al., 2018; Erdmann et al., 2013; Johnstone et al., 1993; Monti et al., 2003; Oemar et al., 1998; Petrie et al., 1996; Sansbury et al., 2012). Here, NOS3 is linked to metabolic disease.