reported that the immunosuppressive state of the TME is ameliorated by PLX3397 through the reduction in the proportion of TAMs, rather than through the induction of their polarization; moreover, the combination of PLX3397 and PD-1 mAbs yielded undesirable anti-tumor efficacy and did not significantly improve the infiltration and activation of T cells; thus, this may be a limitation of this therapeutic approach (108). The gene discussed is PDCD1; the disease is neoplasm.