Interestingly, Bcl-xL overexpression did not prevent the AAP-mediated increase in IL-1β levels (Fig. 8b) but completely prevented its toxic effect on cellular viability (Fig. 8c) suggesting that p65 activation and IL-1β production are events that precede mitochondrial function impairment in AAP-treated neuroblastoma cells. Here, IL1B is linked to neuroblastoma.