HLA-E and myeloid leukemia: Given that myeloid cells are a major target of IFNγ70 and IFNγ promotes myeloid differentiation of HSPC progenitors71, it is possible that myeloid leukemia, in particular, evolves to co-opt IFNγ signaling, ultimately hijacking HLA-E for immune evasion and promoting blast growth in the bone marrow niche.