In the pancreatic cancer model, blockade of CSF1R signaling significantly reduces the number of TAM in the tumor as well as mRNA expression of immunosuppressive molecules such as PD-L2, transforming growth factor-β (TGF-β), and arginase-1 (ARG1) in the remaining TAM (Zhu et al., 2014), suggesting that CSF1R inhibition improves checkpoint therapies not only by depletion of TAM but also by reducing their expression of suppressive molecules. The gene discussed is CSF1R; the disease is neoplasm.