Early reportssuggested a role for NF-κB, but further studies demonstratedthat RIP3−/− cells presented normal NF-κBactivation through TNFα or Toll-like receptorstimulation.19, 20, 21,22 Here we observed that thedeath of DA1-3b leukemia cells induced by RIP3-WT expression was notsignificantly affected in cells that were stably transfected withp65/RelA, I-kappa-B-kinase-beta (IKKβ, or anIKKβSSEE constitutively active mutant (Figure 4a). Here, RELA is linked to leukemia.