Indeed, loss of ATF4 enhances liver damage.29 Unlike HFD-fed BL6 mice, which develop simple or benign steatosis, HFD-fed MUP-uPA mice progress to steatohepatitis, liver damage, and fibrosis owing to ER stress-driven hepatocyte death.7 The results described above suggest that ATF4 attenuates the progression from simple steatosis to NASH and HCC by suppressing ferroptosis, thereby blocking liver damage and necroinflammation. The gene discussed is ATF4; the disease is metabolic dysfunction-associated steatohepatitis.