In this study, our results suggest that palmitate-induced oxidative and ER stress in INS-1 cells were attenuated by IL-22 treatment, which support the previous finding that IL-22 suppressed oxidative and ER stress in mouse and human β cells leading to restoration of insulin secretion [8], and is consistent with evidence suggesting that IL-22 was able to prevent or reverse obesity-induced glucose intolerance and insulin resistance [12]. The gene discussed is IL22; the disease is obesity due to melanocortin 4 receptor deficiency.