In addition, these CKs can activate several serine kinases, including the mammalian target of rapamycin 32 (mTOR32), ribosomal protein S6 kinase, c-Jun N-terminal kinase (JNK), and IκB kinase β (IKKβ) in adipocytes, which further facilitate the suppressive phosphorylation of insulin receptor substrate 1 to cause insulin resistance [50,58]. This evidence concerns the gene IRS1 and Insulin resistance.