For example, in the context of RA, c-IAPs were shown to be functionally involved in TNF-α–induced apoptosis which was traced to the finding that X (cross)-linked inhibitor of apoptosis (XIAP) interacted with mitogen-activated kinase kinase kinase 2 (MEKK2) [55] to alter NF-κB activation. This evidence concerns the gene TNF and rheumatoid arthritis.