The increased Il1r1 expression in these cells could be a result of IL-1β -induced phosphorylation by nuclear IKKa of Ser10 in histone H3 that could be especially important for subsequent modifications in a variety of genes, including Il1r1. Moreover, integrated by IKKα-mediated non-canonical NF-κΒ activity, IL-1β signaling culminates in enhanced CXCL1/PPBP expression and secretion that function to escalate tumor-associated inflammation required for MPE. The gene discussed is IL1B; the disease is neoplasm.