Interestingly, exposure of acute myeloid leukemia (AML) cells to this same TPOR agonist antibody promoted their differentiation into natural killer (NK)-like AML cells that synthesized large amounts of perforin, granzyme B and interferon-γ, and thereby induced apoptosis in undifferentiated AML (Figure 2c) [52]. The gene discussed is PRF1; the disease is acute myeloid leukemia.