Interestingly, they also observed an increase in MHC-II expression and INFγ production, while there was a reduction in the expression of immunosuppressive molecules such as Arg-1 and TGF-β, supporting the hypothesis that CSF-1R targeting does not lead to the depletion of MO-MDSCs, but rather a reorientation of these cells toward an anti-tumor phenotype, thereby favoring T cell-mediated immunity. The gene discussed is CSF1R; the disease is neoplasm.