In patients with autoimmune diseases (such as systemic lupus erythematosus), β2-GPI can activate systemic lupus erythematosus—Th17 and Th1 responses in atherosclerotic lesions in patients with antiphospholipid syndrome—and affect the release of inflammatory factors such as IL-17, IL-12, etc., thereby affecting disease progression (18). This evidence concerns the gene APOH and antiphospholipid syndrome.