In summary, there are multiple pathways by which STAT3 indirectly modulates the function of NK cells, either by the production of tumor-derived immunosuppressive factors, such as IDO, or by driving the development of immunosuppressive myeloid populations, such as MDSCs, which secrete IDO, transforming growth factor (TGF)-β, or other soluble factors that block NK development, cytolytic function, or cytokine production (Figure 1; Table 1). This evidence concerns the gene TGFB1 and neoplasm.