Moreover, high correlation between MUC1 and pSmad3L/c-Myc but not pSmad3C/p21WAF1 expression was also observed in both tumors from nude mice and HCC tissues from patients, suggesting that MUC1 shifts Smad3 signaling from tumor-suppression to oncogenesis in vivo, which is consistent with clinical observations by Matsuzaki et al, which supports the roles for pSmad3L (Ser-213) as a tumor promoter and pSmad3C as a tumor suppressor in virus infection-related HCC tissues [25, 26]. This evidence concerns the gene MYC and neoplasm.