Using the HFD-induced NASH mouse model with short period of P.g.-odontogenic infection (6 weeks), we previously confirmed that P.g.-odontogenic infection exacerbated inflammation/fibrosis of NASH, in which mechanism TLR2 upregulating and/or inflammasome activating by lipid accumulation in hepatocytes contributed to excessive production of proinflammatory cytokines. The gene discussed is TLR2; the disease is metabolic dysfunction-associated steatohepatitis.