Taking this role of AXL/MER into account, blocking their activity could improve antitumor response by (i) increasing pro-inflammatory cytokines and antitumor activity of cytotoxic T cells in tumors with an immunosuppressive environment (high M2 macrophages, low levels of activated CD8 T cells), (ii) simultaneously targeting tumor cells and macrophages in resistant AXL/MER-positive tumors, and (iii) combining TAM inhibitors with immunotherapies to improve antitumor T cell activity by blocking inhibitory checkpoints (e.g., anti-PD1 or anti-CTL4A). Here, AXL is linked to neoplasm.