Together, these results suggest that GPR119/TAK1/NF-κB/TGF-β1 signaling pathway mediates 2-OG-induced MΦ activation in HFS-induced NASH liver, and the resultant TGF-β1 acts as a widely recognized master regulator to activate HSC (Fig. 8). The gene discussed is GPR119; the disease is metabolic dysfunction-associated steatohepatitis.