These results suggest the hypothesis that tumor-associated macrophages and potentially other components of the tumor microenvironment known to produce pro-inflammatory cytokines or other immunologically-active species, such as IFN-γ [60, 61], could have significantly altered gene expression (DUOX2) and signal transduction pathways (ERK) in our pancreatic cancer xenografts. The gene discussed is DUOX2; the disease is neoplasm.