Several studies have revealed that a crosstalk between hypoxia and HH pathways within pancreatic cancer cells is operated in a ligand-independent manner and that the nuclear accumulation of GLI1 could be triggered via other factors, such as TGF-β, K-ras, and receptor tyrosine kinase (RTK) (reviewed in [84]). This evidence concerns the gene TGFB1 and pancreatic neoplasm.