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Additionally, processes involving kappa kinase (IKK-), 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)