IL1B and arthritic joint disease: Similarly, IL-1β stimulated Wnt5a expression through activation of NF- κB and the subsequently overexpression of p65 in chondrocytes, while BAY11–7082, a specific inhibitor of IκBα-phosphorylation, abrogated the induction of Wnt5a by IL-1β in the cartilage destruction caused by arthritis [58].