The production of ROS by B1R-induced activation of NADPH oxidase could represent a putative mechanism by which B1R antagonism reversed the auto-induction of B1R and its pro-inflammatory effects in models of diabetes (Dias et al., 2010; Dias and Couture, 2012a,b; Pouliot et al., 2012). This evidence concerns the gene BDKRB1 and diabetes mellitus.