Selective inhibition of VEGF activation of VEGFR2 with mcr84 increased the expression of adhesion molecules while decreasing expression of FasL on tumor endothelial cells reduced the expression of PD-L1 on myeloid cells, reversed the immunosuppressive phenotype of tumor-infiltrating myeloid cells, and reduced the expression of inhibitory immune checkpoint molecules on TILs. Here, FASLG is linked to neoplasm.