Since the kidney is a major source of eCBs, whose levels are elevated during diabetes and obesity [22,41], and the fact that CB1R, highly expressed in many cells within the kidney, is also upregulated in these conditions [21,22,42,43,44,45,46,47], the possible involvement of the renal eCB/CB1R system in regulating skeletal remodeling and mass in health and disease led us to test the hypothesis that a negative axis, involving CB1R in RPTCs, exists between kidney and bone. This evidence concerns the gene CNR1 and diabetes mellitus.