The results of our study show that the over-expression of Mcm7 during NASH-associated liver carcinogenesis may be explained, at least in part, by activation of c-MYC, YAP1, Wnt/β-catenin, and ERK/MAPK signaling pathways, which was evidenced by increased protein levels of their corresponding transcription factors. The gene discussed is MAPK1; the disease is metabolic dysfunction-associated steatohepatitis.