However, POA-treated HFD-fed mice exhibited lower levels of the liver-damage marker alanine aminotransferase (ALT) (Fig. 2B), less liver steatosis (Fig. 2C), and increased hepatic activation of the anti-inflammatory and pro-oxidative metabolic sensor, AMPK, compared to OA-treated HFD-fed mice (Fig. S1). The gene discussed is GPT; the disease is Hepatic steatosis.