STAT1 and neoplasm: In addition, K562 tumor cells had moderate resistance to the killing of Vγ9Vδ2-T cells in the presence of rhIFNγ and inhibition of STAT1 activation and NO synthesis by fludarabine or 1400 W alleviated the dampened cytotoxic capacity of Vγ9Vδ2-T cells prompted by rhIFNγ (Fig. 6m, n).