In a xenograft model, ablation of the HH co-receptors Gas1 and Boc in mouse embryonic fibroblasts (MEFs) promoted the co-injected human pancreatic cancer cell lines to grow pancreatic tumors, whereas elimination of HH signaling by deletion of Gas1, Boc and Cdon in MEFs inhibited pancreatic tumor growth, indicating a dose-dependent role of HH signaling in differentially regulating pancreatic cancer progression (Mathew et al., 2014). This evidence concerns the gene CDON and familial pancreatic carcinoma.