Specifically, SLC7A11 deficiency accelerated MASLD progression via a classic cystine/cysteine deficiency-induced ferroptosis, while serine deficiency and a resulting impairment in de novo cysteine production were attributed to ferroptosis-induced MASLD progression in mice overexpressing hepatic SLC7A11 [182]. This evidence concerns the gene SLC7A11 and metabolic dysfunction-associated steatotic liver disease.