Histone deacetylase inhibitors (trichostatin A and valproic acid), differentiation-promoting drugs (vitamin D3, bryostatin 1 and all-trans-retinoic acid) and hydroxyurea all somehow show the potential of upregulating the expression of NKG2DLs on AML cells, while dinaciclib-treated AML is associated with the downregulation of inhibitory NK ligand HLA-E on AML cells, consequently inducing potent NK cell anti-tumor immunity [208, 210–213]. The gene discussed is HLA-E; the disease is acute myeloid leukemia.