Because the investigators in those studies demonstrated such a high dependence on STING during chlamydial induction of IFN-β, it was concluded that TLR signaling, MyD88, and TRIF were all dispensable for IFN-β upregulation during chlamydial infection of peritoneal macrophages. The gene discussed is IFNB1; the disease is chlamydia trachomatis infectious disease.