Dysregulated ATP1A1 signaling, influenced by metabolic stress in MASH-related hepatocellular carcinoma (HCC), promotes HCC progression through epigenetic modifications like H3K9 acetylation and tri-methylation, which are linked to decreased autophagy and increased apoptosis when normalized, highlighting ATP1A1 as a potential therapeutic target. The gene discussed is ATP1A1; the disease is hepatocellular carcinoma.