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). The gene discussed is CSF1; the disease is neoplasm.