The impaired intestinal barrier can cause the translocation of infectious factors such as lipopolysaccharide (LPS) and food antigens into the blood, promote various Toll-like receptors to activate NF-κB, further stimulate the massive release of pro-inflammatory factors (IL-1β, IL-6, TNF-α, etc.), and inducing inflammation and insulin resistance of liver, muscle and adipose tissue, leading to the occurrence of type I and type II diabetes (Luissint et al., 2016; Tilg et al., 2020). The gene discussed is NFKB1; the disease is type 2 diabetes mellitus.