As MyD88 is critical for control of L. pneumophila replication during in vivo infection but deletion of an individual MyD88-dependent TLR or a combination of TLRs does not recapitulate MyD88 deficiency, it is likely that other MyD88-dependent receptors, including the IL-1R, may play a role [62]–[66]. This evidence concerns the gene MYD88 and infection.