These previous published results confirmed that SMAD4 has a significant role in the pathogenesis of fibrosis by controlling the ability of SMAD3 to activate transcription of a number of fibrogenic genes (collagens) , markers (α-SMA and E-cadherin)47 and explain the significant overexpression of SMAD4 in NASH group than NC and treated groups observed in the current study (P < 0.001). The gene discussed is ACTA1; the disease is metabolic dysfunction-associated steatohepatitis.