Functionally, we have also demonstrated that DCLK1 regulates key oncogenes, pluripotency factors, angiogenic factors, epithelial mesenchymal transition (EMT) related transcription factors, and pancreatic cancer xenograft growth which can be reversed by downregulating DCLK1 or inhibiting its kinase activity [10–13]. This evidence concerns the gene DCLK1 and familial pancreatic carcinoma.