Furthermore, it has been demonstrated, in an in vivo model of the Chlamydia muridarum infection, the lack of involvement of CD14 (an accessory protein essential for TLR4 recognition) in the immunopathogenesis of the infection, suggesting that TLR4 might not be important for the initial signaling pathway for pro-inflammatory cytokine production during chlamydial infection [38]. The gene discussed is TLR4; the disease is infection.