The lack of correlation between the effects of SMO inhibitors on tumour cell growth and the levels of HH pathway target genes led some investigators to propose that ‘non-canonical’ HH pathway signalling, potentially involving cross-talk with the RAS and TGFβ pathways [84], androgen receptor signalling [85], the mTOR pathway [86] and the WNT pathway [87] among others, contributed to tumour progression. This evidence concerns the gene TGFB1 and neoplasm.