Our data suggests that P.g.-odontogenic infection might accelerate NASH-related neoplastic nodule formation by activating cell proliferation, anti-apoptosis, and cell migration via the integrin β1-signaling pathway such as FAK, AKT and ERK, and by oxidative DNA damage caused by TNF-α produced from increased Mφ that formed hCLS (Fig. 7). The gene discussed is AKT1; the disease is metabolic dysfunction-associated steatohepatitis.