It is reported that pancreatic cancer is characterized by a high degree of infiltration by tumor-associated macrophages (TAMs) that inhibit anti-tumor T-cell activity, and that blocking colony-stimulating factor 1 receptor (CSF-1R) signaling—which supports the recruitment, differentiation, and maintenance of immunosuppressive macrophages in tumors—may lead to depletion of the TAMs and upregulation of T-cell checkpoints. Here, CSF1R is linked to pancreatic neoplasm.