At the cellular level, mechanistic studies revealed that SGB121 and its abundant component F1 mitigate FFA-induced steatosis and oxidative stress by activating AMPK PPARα CPT-mediated β-oxidation, suppressing SREBP1-ACC–FAS-driven lipogenesis, and restoring IRS Akt GLUT2 signaling, thereby improving insulin sensitivity. The gene discussed is FAS; the disease is steatosis.