Additionally, several studies have now determined that eNOS is a downstream effector of EGFR or ErbB2 signaling in T1DM and T2DM (Belmadani et al., 2008; Galan et al., 2012; Benter et al., 2015), and that exaggerated ErbB2-EGFR heterodimerization in the diabetic vasculature leads to diminished NO activity (Benter et al., 2015). This evidence concerns the gene NOS3 and type 1 diabetes mellitus.