IRS1 and Insulin resistance: Additionally, processes involving kappa kinase β (IKK-β), c-Jun N-terminal kinase (JNK-1), protein kinase C (PKC), and mammalian target of rapamycin (mTOR)-driven serine modification of IRS1 also contribute to insulin resistance, further intensified by free fatty acids, lipotoxicity, oxidative stress, and inflammation (Stergios et al., 2009).