Tumors with high AXL expression can be resistant to immunotherapy through increased GAS6 production, decreased HLA-I expression, and release of myeloid-supporting cytokines (M-CSF, CSF2, and CSF3) and chemokines (CCL3 and CCL4) that promote tumor development and progression by recruiting Tregs, MDSCs, and protumorigenic M2 macrophages to the TME [74,75]. The gene discussed is CCL3; the disease is neoplasm.