Having previously established the absence of SHH expression (Shin et al., 2014b) with a low incidence of genetic alterations (Figure 1—figure supplement 1A) and enrichment of mutations in genes involved in epigenetic regulation in human invasive urothelial carcinomas (Cancer Genome Atlas Research Network, 2014a), we compared the level of methylation in the regulatory region of Shh between wild-type bladders and N-butyl-N-4-hydroxybutyl nitrosamine (BBN)-induced urothelial carcinomas. Here, SHH is linked to urothelial carcinoma.