A recent report defined the roles of myeloid cell subsets on the onset and progression of a pancreatic tumor in the context of T-cell-mediated immunity using a syngeneic transplantation model and genetically engineered mouse models (GEMM) where CD11b-DTR mice were backcrossed with mice harboring genetic alterations in Kras/p53/p48 genes [19]. This evidence concerns the gene ITGAM and pancreatic neoplasm.