Although one recent in vitro study found blocking the inhibitory signal (blocking of HLA–KIR) is not so efficient as the activating signal increases (Ara-C treatment that induced NKG2D ligands) potentiate NK cell responses against acute myelocytic leukemia (AML) cells, more in vitro and in vivo studies are needed to demonstrate it. The gene discussed is KLRK1; the disease is acute myeloid leukemia.