Of note, it is inferred that Galectin-9/Tim-3 pathway enhances AML progression via both immune-cell-dependent and immune-cell-independent manners: AML cells take advantage of self-secreted Galectin-9/Tim-3 to attenuate cytotoxic activity of T cells and NK cells; some pathways such as NF-κB, β-catenin, PI3 Kinase/mTOR, and HIF-1 pathways are intrinsically activated with the ligation of Tim-3 by soluble Galectin-9 in human AML cells. The gene discussed is NFKB1; the disease is acute myeloid leukemia.