Romee, Fehniger, and colleagues demonstrated that brief priming with an IL-12, IL-15, and IL-18 cocktail reprogrammed allogeneic NK cells to a cytokine-induced memory-like (CIML) phenotype that endowed them with heightened expansion and persistence in vivo, higher interferon-γ (IFN-γ) production, and enhanced cytotoxicity against AML and other malignancies (13, 104–106). The gene discussed is IL15; the disease is acute myeloid leukemia.