Although the exact mechanism underlying this phenomenon remains unknown, we suggest that EPO, generated by the kidney, is most likely involved, since its role in bone metabolism has been repeatedly demonstrated, and its levels are elevated during diabetes and are explicitly regulated by RPTC-CB1R. From a pharmacological point of view, the antagonism of CB1R in RPTCs has a therapeutic potential in treating diabetes-induced osteoporosis, and in improving the quality of life of patients suffering from diabetes. Here, CNR1 is linked to diabetes mellitus.