In 39 CIDP patients, however, who participated in the largest controlled IVIg trial (ICE trial), the serum levels of the complement activation products C3a, C5a and soluble terminal complement complex (sTCC) were not modulated by IVIg but remained unchanged in patients who responded to IVIg, suggesting that the efficacy of IVIg in CIDP is based on immunomodulatory mechanisms different from complement inhibition [50]. Here, C3 is linked to chronic inflammatory demyelinating polyradiculoneuropathy.