However, previous studies have shown that AS is an autoimmune disorder that is associated with Th17 cells and immune pathways, including the interleukin- (IL-) 17/IL-23 pathway [51, 52], and Th17 cells derived from CD4+T cells can release various kinds of cytokines, such as IL-17A and IL-22, which result in bone erosion/proliferation in AS [3], whereas the differentiation of Th17 cells is influenced by multiple inflammatory cytokines, including IL-1β, IL-6, TGF-β, and IL-23 [52]. The gene discussed is TGFB1; the disease is autoimmune disease.