INTRODUCTIONrnAnkylosing spondylitis (AS) is an autoimmune disease that mainly affects the spine and sacroiliac joint with a progressive increase in the stiffness of soft tissues, including ligaments, as a common type of spondyloarthritis. The prevalence rates of AS are estimated to range from 0.1％ to 0.32％ worldwide. Affecting nearly 1.3–1.6 million patients in Europe and 4.6–5.0 million patients in Asia, this disease more commonly occurs in North America with a prevalence of 31.9 per 10000 of the population.1 The inflammation often leads to calcification and bone formation with destructive bone lesions, resulting in spinal fusion, loss of flexibility, and chronic back pain. Significant progress in understanding the cause of this autoimmune disease and developing treatment for inflammation has been achieved in the last decade.2 Immune cells and innate cytokines, particularly the human leukocyte antigen (HLA)?B27 and interleu-kin?23/17 axis, are crucial in the pathogenesis of AS. Since its discovery, HLA-B27 has been considered the major genetic risk factor for AS.3 Advances in the study of autoimmune diseases and anti-inflammatory treatments have not slowed ankylosis mainly because of the limited understanding of how inflammation induces fusion of axial joints.