In contrast, aspartate labeling from glutamine tracer shows that arginase 2 (Arg2) deletion in the mitochondrial urea cycle impairs TCA cycle flux, prompts compensatory glutamine anaplerosis, and predisposes to age-induced MASLD and MASH in mouse models, MASH-derived human organoids, and in prospective human metabolomic studies. The gene discussed is ARG2; the disease is metabolic dysfunction-associated steatotic liver disease.