Following the observation that IFNγ-induced activation of STAT1 is attenuated in Chlamydia-infected A2EN polarized cervical epithelial cells (20), we sought to characterize the basis and significance of this observation in a more physiologically relevant context by lowering the level of exogenously added IFNγ and adjusting the timing of treatment to reflect an already established infection. The gene discussed is STAT1; the disease is infection.