For the vascular and renal complications of diabetes, evidence for a protective role of kinins and B2R comes from the observation of aggravated diabetic nephropathy in several animal models sharing the absence of B2R activation secondary to either inactivation of the B2R gene or reduced bioavailability of endogenous kinins in tissue kallikrein knock-out mice [29] or mice expressing three copies of the ACE /kininaseII gene [83]. The gene discussed is ACE; the disease is diabetic kidney disease.