The objective of our study was to determine 1) whether deletion of B2-receptors will result in alteration in specific gene expression profiles whose specific functions can shed light on the role(s) of B2-receptors, and 2) whether diabetes will result in differences in the patterns of gene expression and pathways between B2R+/+D and B2R−/−D mice that can be linked to the pathological manifestation observed after the induction of DN. Here, BDKRB2 is linked to diabetes mellitus.