Abnormalities in any link in this pathway, leading to impaired insulin receptor signaling, can lead to insulin resistance.[53] While high levels of ROS can inhibit the activation of AKT directly or activate JNK to inhibit IRS1/2 autophosphorylation indirectly to cause insulin resistance.[53, 54] Overall, physiological ROS levels can effectively promote insulin secretion of β cells and insulin sensitivity of some key tissues, while insulin resistance and β cell apoptosis are closely related to excessive ROS. This evidence concerns the gene IRS1 and Insulin resistance.