In breast cancer cells GTT inhibited the nuclear factor kappa beta (NF-κB) activation pathway, leading to the down-regulation of various NF-κB-downstream targets that support cell survival (IAP1, IAP2, Bcl-xL, Bcl-2, cFLIP, XIAP, Bfl-1/A1, TRAF1, and survivin) and proliferation (cyclin D1, COX2, and c-Myc) besides potentiating apoptosis [13]. This evidence concerns the gene NFKB1 and breast cancer.