This model revealed that liver‐specific Arid1a deficiency induced nonalcoholic steatohepatitis[10, 11] and promoted hepatocellular carcinoma (HCC) in mice.[12, 13] Paradoxically, Arid1a deletion has also been reported to enhance liver regeneration[14] while inhibiting tumor initiation yet accelerating HCC progression and metastasis,[15] indicating context‐dependent roles for Arid1a in liver cancer.[16] These findings suggest that Arid1a mutations in chronic liver diseases may drive liver tumorigenesis under specific environmental exposures. The gene discussed is ARID1A; the disease is metabolic dysfunction-associated steatohepatitis.