No changes in any of these parameters were found in the diabetic RPTC-CB1−/− animals (Figure 2M–P), suggesting that knocking out CB1R in RPTCs protects the animals from the deleterious effects of hyperglycemia on both trabecular and cortical bone, and preserves their biomechanical properties and resistance to diabetic fractures. The gene discussed is CNR1; the disease is Hyperglycemia.