KLRK1 and acute myeloid leukemia: To counteract escape mechanism of AML like downregulation of NKG2D ligands [13], NKG2D receptor induction in NK cells by ex vivo expansion [35, 36] or in vivo expansion plus activation by applied cytokines [34, 37], and on the other hand induction of NKG2D ligands on AML target cells by all-trans retinoic acid, the histone deacetylase inhibitor sodium valproate or spironolactone might increase clinically relevant NK mediated antitumor effect [38–41].