SMO and basal cell carcinoma: However, we cannot exclude the possibility that divergent phenotypes could be due to different functions of SmoM2 [an allele identified in human basal cell carcinoma (Xie et al., 1998)] versus endogenous Smo. The phenotypic differences between SmoM2 conditional expression and Ptch1 loss in the mammary epithelium agree with the lack of canonical hedgehog target gene upregulation in Ad-Cre;Ptch1fl/fl ducts, and the inability of IPI926 to block hyperproliferation (Figs 1, 2), suggesting that hyperproliferation is SMO independent.