Inhibition of iNOS for 1-week with 1,400 W (N- (3-aminomethyl-benzyl acetamidine) (Haddad and Couture, 2016) or B1R with SSR240612 (Dias et al., 2010; Dias and Couture, 2012a,b) reversed insulin resistance and its associated metabolic features (hyperglycemia, hyperinsulinemia) through the inhibition of the oxidative stress and the nuclear factor NF-κB pathway leading thereby to the concomitant suppression of CPM, B1R, iNOS, and IL-1β overexpression. Here, BDKRB1 is linked to hyperinsulinism.