The above sections point to MERTK (and the other two TAM RTKs) as potential therapeutic targets by at least two mechanisms: (1) Inhibition of these RTKs in the tumor cell itself abrogating growth, survival, and chemo-resistance mechanisms and (2) Acting to reverse the myeloid cell immune-suppressive mechanisms making T-cell checkpoint therapy more efficacious (Figure 3). This evidence concerns the gene MERTK and neoplasm.