INS and metabolic disease: It does not block CDK5-mediated phosphorylation of Rb but inhibits the TNF-α-mediated phosphorylation of PPARγ in adipocytes, suggesting that PPARγ could be selectively directed and significantly improved insulin sensitivity in high-fat-fed mice without causing significant side effects, which means it could be a potential therapeutic agent for T2D and related metabolic diseases [39].