Not only does Salp20 inhibit properdin function, it actively dissociates properdin from alternative pathway convertases.182 Salp20 inhibits LPS‐induced alternative pathway activity in vivo in mice and ameliorates disease pathogenesis in murine models of OVA‐induced asthma and AAA,103 and thus it is an excellent starting point for the future development of potent, non‐immunogenic human properdin inhibitors. This evidence concerns the gene CFP and asthma.