The results of this study are consistent with what we previously observed in a mouse model of hyperglycemia-induced atherosclerosis, the ApoE−/−:Ins2+/Akita rodent model, where ovariectomy significantly changes the glycemic phenotype with ovariectomized female ApoE−/−:Ins2+/Akita mice which remain chronically hyperglycemic and show signs of UPR activation [9, 10, 25]. The gene discussed is APOE; the disease is Hyperglycemia.