Functional studies in the absence and presence of leukemia cell lines and primary AML cells as targets and PBMC of healthy donors as effectors revealed the profound capacity of NKG2D-CD16 and NKG2D-CD3 to stimulate NK cells and T cells, respectively, as shown by analyses of activation, degranulation, granzyme B and perforin levels, IFN-γ secretion and target cell lysis in an allogeneic and notably also an autologous setting. The gene discussed is PRF1; the disease is acute myeloid leukemia.