NFKB1 and acute myeloid leukemia: In the B16 mouse melanoma tumor model, TNFAIP3 silencing in DCs resulted in an augmented amount of tumor-specific cytotoxic T cells (187); in AML, TNFAIP3 depletion in AML-DCs potentiated autologous cytolysing T cell (CTL)-specific killing of progenitor AML cells via the NF-κB pathway (188).