In this regard, investigating the efficacy of EF24 in disrupting the IR-induced molecular signal transduction (here in this case, NFκB-TNFα cross-signaling), inhibiting persistent activation of NFκB, and, reverting induced survival advantage, clonal expansion, NB dissemination to distant sites in response to IR will prove highly beneficial in achieving the desired therapeutic gain in treating NB. The gene discussed is TNF; the disease is neuroblastoma.