Given that B1R can activate iNOS through Gαi, Gβγ and Src-dependent activation of the ERK/MAP kinase pathway to generate high level of NO (Kuhr et al., 2010), one can suggest that peroxynitrite (ONOO−) generated from the combination of NO and O2•- (Johansen et al., 2005) can contribute to the detrimental effect of B1R and to the reduction of endothelium-derived NO bioavailability in diabetes (Couture et al., 2014; Haddad and Couture, 2016). The gene discussed is BDKRB1; the disease is diabetes mellitus.