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In humans, strains of<jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>cause trachoma, chlamydia, and lymphogranuloma venereum. These diseases are all associated with extended courses of infection and reinfection that likely reflect the ability of chlamydiae to evade various aspects of host immune responses. Interferon-stimulated genes, driven in part by the cytokine interferon gamma, restrict the host range of various<jats:named-content content-type=\"genus-species\">Chlamydia<\/jats:named-content>species, but how these pathogens evade interferon-stimulated genes in their definitive host is poorly understood. Various<jats:named-content content-type=\"genus-species\">Chlamydia<\/jats:named-content>species can inhibit death of their host cells and may have evolved this strategy to evade prodeath signals elicited by host immune responses. 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