Although the basis for caspase-1 stimulation of chlamydial infection is not well defined [32] and remains poorly characterized in our human synovial cell model, we found that exposure of C. trachomatis-infected cells to IFN-γ may modulate the canonical inflammasome pathway by reducing the gene expression of caspase-1. The gene discussed is IFNG; the disease is chlamydia trachomatis infectious disease.