So, many different downstream pathways lead to formation of an IKK complex which then phosphorylates IKb-a; which is bound to NF-κB in its inactive state. The phosphorylation leads cellular proteases to destroy the phosphorylated IKb-a, bonded to NF-κB. The IKb-a is bound to NF-κB when inactive. The phosphorylation allows the IKb-a to detach from NF-κB. The NF-κB (alone, now) can now enter the nucleus and bind to DNA. NF-κB transcribes mRNA which is then translated, making inflammatory proteins, furthering inflammation .

Side note: Doesn't aspirin work by inhibiting IKb-b (NSAID) which stops COX production?