Specifically, we and others have shown that pharmacological blockade or genetic deletion of CB1R in RPTCs protects the kidney from the deleterious effects of hyperglycemia (in T1D and T2D) and/or fatty acid flux (obesity), and ameliorates diabetes- and obesity-induced albuminuria, fibrosis, and renal inflammation [19,20,21,22,39,40]. This evidence concerns the gene CNR1 and obesity due to melanocortin 4 receptor deficiency.