17a has shown maximized cell death, restricted osteoclast genesis-constrained penetration via NF-κB route destruction, and NF-κB-Snail-RKIP interruption, resulting in suppression of antiapoptotic genetic variants and conversion to mesenchymal from epithelial cells [149,150,151]; and it initiated caspase-8 and ROS-dependent apoptotic cell death in leukemia [152]. The gene discussed is NFKB1; the disease is leukemia.