Tim-3 released by AML—reduce ability of T cells to secrete IL-2 required for NK and CTLs activation (99). TIM-3 and PD-1 co-expression on T cells was associated with AML progression in mouse and human (7) and with relapse in AML patients after allo-SCT (100). TIM-3—overexpression on AML (stem) cells (101) and T cells of newly diagnosed AML -(102). Blocking of TIM-3 and PD-1—reduced tumor burden and improved survival in AML murine model (7). The gene discussed is HAVCR2; the disease is neoplasm.