In this study, we showed that (1) palmitate, a saturated fatty acid, elevated serum ALT levels in the presence of gut-derived endotoxin, (2) palmitate induced inflammatory cell infiltration in the liver by up-regulation of chemokines and stimulated mild liver fibrosis via the TLR4 pathway despite the absence of endotoxin, (3) palmitate lipotoxicity cooperated with gut-derived endotoxin in liver inflammation, and (4) fibrosis was also confirmed in patients with NAFLD (Fig. 6). The gene discussed is GPT; the disease is inflammation.