Although constitutively-active in PDA and PDA cell lines, non-canonical activation of the p52/RelB NF-κB complex seems independent of oncogenic KRas11, and is mediated through proteasomal downregulation of TNF receptor-associated factor 2 (TRAF2) and subsequent stabilization and activation of NF-κB-inducing kinase (NIK)9. This evidence concerns the gene RELB and Patent ductus arteriosus.