The P53‐MDM2 axis is crucial for balancing cellular responses to stress.[17] In MASH, P53 is activated in response to oxidative stress and lipid accumulation, regulating hepatic lipid metabolism, apoptosis, and fibrosis.[18, 19] Dysregulation of the P53‐MDM2 interaction in MASH can exacerbate disease progression, with MDM2 overexpression linked to increased liver fibrosis.[20] Studies support that P53 activation in MASH correlates with liver apoptosis and inflammation. Here, MDM2 is linked to Hepatic fibrosis.