As outlined in Figure 2B, stimulated tumor cells, in a cell type specific manner, re-activate Hh signaling, which can be achieved by activating mutations in canonical Hh signaling receptor proteins Smo and Ptch, or non-canonically through other signaling pathways that lead to Gli activation such as TGFβ, PI3K/AKT, ERK and others. This evidence concerns the gene SMO and neoplasm.