There is no conclusive evidence that ankylosing spondylitis is a genetic disease, but 90% of people with ankylosing spondylitis have a genetic component. Therefore, ankylosing spondylitis is a disease that is closely related to genetics. Moreover, after a lot of research and observation, the cause of AS has not been fully elucidated yet, and most of them believe that genetics, infection, and immune environmental factors are related. Genetic factors have an important role in the development of AS. According to epidemiological surveys, the rate of HLA-B27 positivity in AS patients is as high as 90%-96%, while the rate of HLA-B27 positivity in the general population is only 4%-9%; the incidence of AS in HLA-B27 positive patients is about 10%-20%, while the incidence in the general population is 1‰-2‰, a difference of about 100 times. It has been reported that the risk of AS in a group of relatives is 20 to 40 times higher than that of the general population, and the prevalence of AS in first-degree relatives is 24.2% in a domestic survey, which is 120 times higher than that of the normal population. the chance of AS in relatives of HLA-B27-negative healthy people is much lower than that of relatives of HLA-B27-positive AS patients. All these indicate that HLA-B27 is an important factor in the development of AS. However, it should be noted that, on the one hand, not all HLA-B27-positive individuals develop spondyloarthropathy, and on the other hand, approximately 5% to 20% of patients with spondyloarthropathy test negative for HLA-B27, suggesting that other factors besides genetics influence the development of AS. Therefore, HLA-B27 is an important genetic factor in the expression of AS, but it is not the only factor affecting the disease. There are several hypotheses to explain the joint between HLA-B27 and spondyloarthropathies: ① HLA-B27 acts as a receptor site for an infectious factor; ② HLA-B27 is an indigenous modification of an immune response gene that determines susceptibility to environmental excitatory factors; ③ HLA-B27 can cross-react with foreign antigens, thereby inducing the development of tolerance to foreign antigens; ④ HLA-B27 enhances neutrophil leukocyte motility. With the help of monoclonal antibodies, cytotoxic lymphocytes, immunoelectrophoresis and restrictionfragmentlengthpolymorphism, about 7 or 8 subtypes of HLA-B27 have been identified. There may be genetic differences between healthy HLA-B27-positive individuals and patients with spondylosis, for example, all HLA-B27 individuals have a constant HLA-B27M1 antigenic determinant cluster, and antibodies against this antigenic determinant cluster can cross-react with HLA-B27. Most HLA-B27 molecules also have an M2 antigenic determinant. HLA-B27M2 negative molecules appear to be more strongly associated with AS than other HLA-B27 subtypes, especially in Asians, and HLA-B27M2-positive subtypes may have an increased susceptibility to Reiter syndrome. It has been shown that two antigenic determinants, HLA-B27M1 and M2, and the arthropogenic factors Saurobacter, Shigella, and Narsenia can cross-react. Those with a low response seem to present mostly with AS, while those with an increased response develop reactive arthritis or Reiter’s syndrome.