In addition, data from in vivo infection models demonstrated that TLR2 knockout mice had a more severe disease, as well as an intense and prolonged chlamydial infection, as compared to wild type mice, and TLR3 and STING played a key role in the activation of a multitude of inflammatory modulators [32,33,34]. The gene discussed is TLR2; the disease is chlamydia trachomatis infectious disease.