Thus, pancreatic tumor induction and progression in patients is due to not only combined defects in NK expansion, decreased NK-cell mediated cytotoxicity and lower secretion of IFN-γ, and much lower ability of secreted IFN-γ to differentiate tumors, but also due to the defects in other subsets of immune cells which support NK cell expansion and function. This evidence concerns the gene IFNG and pancreatic neoplasm.