In 2014, mice lacking Gpx4 were shown to develop spontaneous acute renal failure and hepatic I/R-induced damage via ferroptosis.5 Subsequently, the pathogenic role of ferroptosis in the progression of I/R-induced acute damage in the lungs, heart, and intestinal tract has been validated in animal models.3,4,59 We previously systematically reviewed the varied role of ferroptosis in liver disease, and we refer the reader to this review.60 Notably, tissue-specific Gpx4 knockout mice present with tissue damage accompanied by massive death of photoreceptor cells61 and endothelial cells.62 This evidence concerns the gene GPX4 and liver disorder.