Metabolic dysfunction-associated steatotic liver disease (MASLD) covers a series of pathogenic conditions including steatosis, inflammation and fibrosis with limited therapeutic options to date. Recent findings have shown upregulation of hepatic murine double minute 2 (MDM2) in patients with MASLD. Additionally, genetic deletion of hepatic MDM2 and its pharmacological inhibition were seen to improve steatosis and fibrosis in MASLD murine models.