SLC7A11 deficiency accelerates the progression of high-fat diet-induced MASLD through ferroptosis induced by classical cystine/cysteine deficiency, while serine deficiency and consequent obstruction of de novo synthesis of cysteine are responsible for the progression of ferroptosis induced MAFLD in hepatic SLC7A11 overexpressing mice.305 These results suggest that liver cells require a narrow window of SLC7A11 activity to maintain healthy liver function when exposed to a high-fat environment. This evidence concerns the gene SLC7A11 and metabolic dysfunction-associated steatotic liver disease.