The defects in glucose homeostasis in Ocn−/− mice are accompanied by impaired pancreatic β-cell proliferation and insulin secretion and the development of insulin resistance in other insulin-target tissues.6 While the hypoinsulinemia observed in our Rptorob−/− mice may be attributed to low serum levels of unOCN, GSIS tests indicated maintenance of ability to secrete insulin in response to glucose in the Rptorob−/− mice. Here, BGLAP is linked to Insulin resistance.