In summary, MET signaling is assumed to inhibit tumor immune responses by increasing PD-L1 expression, promoting the differentiation of T-cells into Tregs, increasing immunoinhibitory enzyme IDO-1 activity, and promoting the production of the immunosuppressive cytokine TGF-β [31, 32] AXL signaling is assumed to inhibit the antitumor activity of activated macrophages, dendritic cells, and NK cells [33, 34]. This evidence concerns the gene MET and neoplasm.