Like human HCC tumor specimens, Hep3B had significantly higher levels of SMO than PTCH1, and treatment of Hep3B with KAAD-cyclopamine (antagonist of oncogenic mutant SMO) but not cyclopamine (antagonist of wild-type SMO) markedly repressed GLI1 activity, suggesting that genetic alteration of SMO can promote HCC carcinogenesis through GLI1 activation. Here, GLI1 is linked to neoplasm.