It has been known that low levels of cellular ROS are required for cellular signaling, such as optimal tyrosine phosphorylation-dependent signaling in vitro (49–51), while chronic excessive generation of ROS aggravate insulin sensitivity in skeletal muscle and disrupt β-cell function and survival (52), suggesting that an optimal balance of cellular redox regulation is critical for the pathogenesis of both T1DM and T2DM. The gene discussed is INS; the disease is type 1 diabetes mellitus.