The pro-inflammatory effect of resistin may be mediated by binding to Toll-like receptor 4 (TLR4) and the subsequent activation of NF-κB in macrophages via the c-Jun N-terminal kinase (JNK) and p38 MAPK pathways; these contribute to the development of insulin resistance and inflammation, closely related to obesity and associated metabolic diseases [61,62]. The gene discussed is TLR4; the disease is Insulin resistance.