Our data demonstrate that chronic TGFβ imprinting in conjunction with activation and IL-2 has opposite effects of acute TGFβ exposure (6 h to 3 days), driving NK cells to produce more IFNγ and TNFα upon tumor target and PHA stimulation than NK cells that were not TGFβ imprinted [18,19,21,31]. The gene discussed is TGFB1; the disease is neoplasm.