Mitochondrial dysfunction and subsequent excess ROS production promotes insulin resistance through activation of the c-Jun amino-terminal kinase (JNK) and NLRP3 inflammatory vesicles, leading to the inactivation of the insulin receptor substrate (IRS)1/PI3K/serine/threonine kinase (Akt) pathway, which promotes insulin resistance progression (78). Here, IRS1 is linked to Insulin resistance.