CSF1R and neoplasm: The predominance of an M2 phenotype in our data echoes the central dependence of M2 TAMs on CSF-1/CSF-1R signaling: blockade of CSF-1R (e.g. with pexidartinib or PLX3397) is known to reprogram or deplete TAMs, modulate the tumor immune microenvironment, and inhibit sarcoma growth in preclinical models, lending translational rationale to our findings (43).