The TLR4 activation by binding to myeloid differentiation factor 88 (MyD88) can activate the downstream (NF-κB), induce the product of pro-inflammatory/inflammatory factors, and result in glucolipid metabolism disorders, while TLR4-specific deletion can improve insulin resistance and glucose tolerance, depress the differentiation of preadipocyte, and decrease the accumulation of lipids [15,36]. The gene discussed is NFKB1; the disease is Insulin resistance.