The different mechanisms of immune evasion post allo-HCT are shown in 6 major categories. (1) Impaired leukemia cell recognition via genomic loss/impaired expression of HLA or defects in the antigen (Ag)/HLA-presentation machinery.^11,84  (2) Upregulation of immune-checkpoint molecules: a role for programmed death 1 (PD-1) is shown for Hodgkin lymphoma and the B7 family member/CTLA4 axis is shown in clinical trials; hypothetically, CD155, VISTA, B7-H3, B7-H4, and others could play a role in AML immune escape post allo-HCT.^28,85  (3) Increased anti-inflammatory cytokine production was shown in leukemia cells, which could hypothetically play a role in relapse; examples are interleukin-10 (IL-10) and transforming growth factor β (TGF-β). (4) Reduced production of IL-15 was shown to lower anti-AML immune responses post allo-HCT.⁴¹  Hypothetically, suppression of other cytokines such as granulocyte colony-stimulating factor (G-CSF), which promotes Ag-presenting cell (APC) maturation, could play a role in AML immune escape post allo-HCT. (5) Production of the metabolic active molecules CD73, indoleamine 2,3-dioxygenase (IDO), and arginase by leukemia cells was shown and CD73 deletion or inhibition promoted graft-versus-leukemia (GVL) effects in the mouse model.⁵¹  These molecules could play a role in AML immune escape. (6) Acquisition of novel oncogenic mutations and loss of tumor-suppressor genes post allo-HCT have been described.^7,52-54  Hypothetically, this increased proliferation could promote immune escape as leukemia cells outnumber T cells and NK cells. FLT3-ITD, FLT3–internal tandem duplication; PD-L1, programmed death ligand 1.