The mechanism by which Tim-3 mediates inhibitory signaling remains unclear, and several mechanisms are suggested that Tim-3 may promote tumor progression, including facilitating tumor cell migration and invasion, activation of the IL-6-STAT3 pathway leading to direct suppression of CD4 + T cells to inhibit Th1 polarization or activation of mTOR function in AML cells. Here, HAVCR2 is linked to acute myeloid leukemia.