CD4-positive T cells recognize this abnormal homodimer and produce IFN-γ and IL-17.[14] These cytokines activate monocytes, macrophages, osteoblasts, synovial fibroblasts, and vascular endothelium to release inflammatory cytokines such as IL-6 and TNF-α.[15] Our patient had been suffering from gouty arthritis with hyperuricemia for years, and he subsequently had Chlamydia infection that triggered ReA. The gene discussed is IL6; the disease is hyperuricemia.