Notably, despite supporting near-normal chlamydial GT infectious loads, P2X7R−/− and TNFR1/2−/− mice exhibited significantly reduced GT pathology (Fig. 6f), showing the P2X7R signaling pathway is critical for the development of CtD GT pathology. The gene discussed is TNFRSF1A; the disease is Glanzmann thrombasthenia 1.