Treatment with inhibitors of histone deacetylase (HDACi) and DNA methyltransferase (DNMTi) was found to restore NKG2DL (MICA and ULBPs 1–3) expression in AML through the hypomethylation of TIMP3, an inhibitor of protease ADAM17, the sheddase involved in the release of soluble NKG2DL by AML cells [105]. The gene discussed is ADAM17; the disease is acute myeloid leukemia.