Dysregulated AMPK activity—characterized by reduced phosphorylation—is a hallmark of NAFLD pathogenesis, driving excessive de novo lipogenesis, impaired fatty acid oxidation, inflammasome activation, and mitochondrial dysfunction, all of which exacerbate hepatic steatosis and injury (He et al., 2024; Lv et al., 2024; Liu et al., 2023). Here, PRKAA1 is linked to metabolic dysfunction-associated steatotic liver disease.