The translocation from the oral cavity to the gut of of P. gingivalis, including its lipopolysaccharide (LPS), can promote gut dysbiosis and inflammation by upregulating toll-like receptor 2 (TLR2), tumor necrosis factor alpha (TNF-α), and interleukin-17 (IL-17), also contributing to hepatic inflammation and liver fibrosis in metabolic dysfunction-associated fatty liver disease [24]. The gene discussed is IL17A; the disease is fatty liver disease.