When hepatocytes were exposed to chemical carcinogen, and when tumor cells in hepatocellular carcinomas were under metabolic stress induced by genomic instability, MAP1S was dramatically elevated and activated autophagy to degrade P62-associated protein aggregates and dysfunctional mitochondria, eliminate g-H2AX-labeled DNA double-strand breaks and suppress genomic instability. The gene discussed is MAP1S; the disease is hepatocellular carcinoma.