INS and Insulin resistance: For instance, pro-inflammatory cytokines involved in the activation of IκB kinase beta (IKK-β)/nuclear factor kappa B (NF-κB) and c-Jun N-terminal kinase 1 (JNK1) pathways cause serine kinase phosphorylation of IRS-1 or IRS-2, which attenuate insulin signaling and consequently leads to the development of insulin resistance [140].