However, in the PDAC mouse model with oncogenic Kras expression, conditional deletion of Smo in ductal cells does not affect GLI1 expression in cancer cells and had no effects on the multistage development of PDAC tumors [36], indicating that ligand-receptor Hh signaling is dispensable in pancreatic ductal cells for PDAC progression, and GLI transcription in the neoplastic ductal cells is regulated through alternative manners. The gene discussed is KRAS; the disease is cancer.