In an autochthonous murine model of N-butyl-N-4-hydroxybutyl nitrosamine (BBN) carcinogen-induced urothelial cancer, genetic loss of Smo in GLI1-expressing stromal cells led to loss of pathway activation in stromal cells, accelerated tumor growth, decreased survival, and loss of the differentiation factors, BMP4 and BMP5, in stromal cells [74]. This evidence concerns the gene GLI1 and neoplasm.