In tissue-specific Rubicon-deficient mice, the development of nonalcoholic fatty liver disease was suppressed6, aging phenotypes in the kidney and the brain7 via the stimulation of autophagic activity were reduced, and cardiac ischemia/reperfusion injury was attenuated8, indicating the detrimental effect of Rubicon. The gene discussed is RUBCN; the disease is metabolic dysfunction-associated steatotic liver disease.