Recently, we reported that circulating XOR in humans and mice markedly increased with elevations in liver enzymes such as serum alanine aminotransferase (ALT) or aspartate aminotransferase (AST), reflecting excessive leakage of hepatic XOR, and that topiroxostat, a selective XOR inhibitor, suppressed plasma XOR activity and attenuated the development of vascular neointima formation in a diet-induced mouse model of NAFLD/NASH [12,13]. The gene discussed is GPT; the disease is metabolic dysfunction-associated steatohepatitis.