Moreover, a mechanistic leap in our understanding of macrophage-specific targeting of the CSF1/CSF1R axis has been achieved in murine models of pancreatic ductal adenocarcinoma (137, 196); in fact, PD1 and CTLA4 antagonists showed limited efficacy as single agents to restrain tumor growth, but in combination with CSF1R blockade potently elicited tumor regressions, even in larger established tumors, providing a rationale to fuel the subsequent efforts to translate CSF1/1R-specific and other tumor-associated macrophage modulating therapies into the clinic (196). The gene discussed is CSF1; the disease is neoplasm.