Although the specific mechanisms behind insulin resistance are not fully understood, it has been shown that pro-inflammatory signals and inflammation, such as TNF-a, IL-1B, inhibitor of nuclear factor kappa B kinase subunit beta (IKBKB commonly known as IKKbeta), c-Jun N-terminal kinase (JNK), and NLPR3 inflammasome, are capable of disrupting insulin signaling in adipocytes or muscle cells (20). This evidence concerns the gene TNF and Insulin resistance.