Moreover, CB1R genetic deletion reduces TNFα secretion by Kupffer cells,30 and pharmacological CB1R antagonism or its genetic deletion inhibits TNFα expression in diabetic cardiomyopathy.31 Moreover, we have previously shown that peripheral CB1R antagonism or its genetic deletion from renal proximal tubule cells normalizes the elevated TNFα levels in both type 1 diabetes and diet-induced obesity mouse models.32,33 In agreement with all of these studies, we show here that peripheral CB1R antagonism also normalizes bladder TNFα levels as well as systemic inflammation. The gene discussed is TNF; the disease is type 1 diabetes mellitus.