PLB was also a potent inhibitor of the NF-κB signaling pathway and suppressor of T-ALL cell proliferation, because PLB induced caspase-dependent apoptosis of MOLT-4 cells and inhibited LPS-induced phosphorylation of p65, and the transcription of NF-κB target genes[36]. This evidence concerns the gene NFKB1 and acute lymphoblastic leukemia.