IFNγ, granulocyte-colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) increased the expression of CD64 on monocytes and enhanced their cytotoxic potential.32 Treatment of target cells with IFNγ also increased their killing by the bispecific antibody.33 Although the treatment of AML cells with monospecific anti-CD33 or anti-CD64 antibodies for 48 h inhibited AML cell growth, the inhibitory potency mediated by the bispecific molecule was higher. The gene discussed is FCGR1A; the disease is acute myeloid leukemia.