Together, these results show that i) canonical HH signaling in cSCC cell lines is neither inducible with SHH or SAG nor inhibitable with cyclopamine or vismodegib, at least under our experimental conditions and ii) that the SMO inhibitor HhA can paradoxically induce the expression of GLI1, which has also been seen in other tumor cell lines (Ridzewski et al., 2015). This evidence concerns the gene GLI1 and neoplasm.