We previously showed inducible suppression of bone turnover markers (BTMs) in insulin‐sensitive subjects with supraphysiological levels of insulin, suggesting that hyperinsulinemia drives bone turnover suppression in T2D.(18) However, more severe hyperglycemia has not been consistently associated with lower BTMs(19, 20) or higher fracture risk.(21, 22) It is therefore unclear how obesity, IR, and VAT independently and cumulatively relate to bone metabolism and fracture risk within T2D individuals. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.