Furthermore, data obtained from Pdia4 knockout and transgenic mice showed that Pdia4 promoted β-cell failure, including cell death and dysfunction, and diabetes via up-regulation of ROS production as indicated by fasting blood glucose (FBG), postprandial blood glucose (PBG), glycosylated hemoglobin A1c (HbA1c), glucose tolerance test (GTT), islet architecture, diabetic incidence, and homeostatic model assessment for β-cell function and insulin resistance (HOMA) indices. The gene discussed is PDIA4; the disease is diabetes mellitus.