Experimental investigations using dual genetic ablation models revealed that combined deletion of PTEN (phosphatase and tensin homolog) and Salvador homolog 1 (SAV1) establishes pathological synergy between YAP/TAZ mechanotransduction pathways and AKT/IRS2 nutrient-sensing cascades, precipitating non-alcoholic fatty liver disease onset and ultimately promoting hepatocellular carcinogenesis [36, 37]. The gene discussed is PTEN; the disease is metabolic dysfunction-associated steatotic liver disease.