Upon induction of senescence in a cancer line of mesenchymal origin (osteosarcoma, U2-OS), phosphorylation of NF-κB subunit p65 by GSK3β paves the way to a persistent SASP because it represses transcription of IκBα, which otherwise acts as the negative feedback loop restricting NF-κB activity [97]. This evidence concerns the gene NFKB1 and cancer.