In keeping with this observation, TIFA silencing increased chemotoxicities of both AML cells and patient-derived peripheral blood mononuclear cell (PBMC) via inhibition of inflammatory cytokines secretion, leading to tumor necrosis factor α (TNFα)-dependent NF-κB survival pathway attenuation and, thus identifying TIFA as a potential target in AML [23]. This evidence concerns the gene NFKB1 and acute myeloid leukemia.