A research showed the same effect in colon and breast cancer mouse models, where the co-blockade of CTLA-4 and CSF1/CSF1R enhanced the beneficial effect by significant reduction in the number of tumor-infiltrating M-MDSCs, not PMN-MDSCs, and reprogramming M-MDSCs that displayed markedly increased expression of MHC class II and reduced expression of the immunosuppressive molecules ARG1 and TGF-β (146). Here, CTLA4 is linked to neoplasm.