In the national planning textbook, there is a chapter dedicated to rheumatoid arthritis, from onset to clinical manifestations, to diagnosis, differential diagnosis and medication, which is very comprehensive. Most of the content is of interest to patients with rheumatoid arthritis, and many of them mention the causes of the disease: Why do I have rheumatoid arthritis? Is it genetic? Is it hereditary? Or is it something cold or wind? Or did you eat something wrong? The causes of rheumatoid arthritis have always been a mystery, and we can only guess: genetics? Infection? Wind and cold? Eating the wrong things? The list goes on and on. Experts and scholars around the world are constantly researching and in recent years have found many new clues to further unravel this mystery. The first thing to talk about is environmental factors, the first thing that comes to mind is the cold weather, getting cold and so on. But the textbook does not seem to take these as the focus. It is generally accepted that changes in the weather can affect the clinical symptoms of patients, but the involvement in the development of rheumatoid arthritis seems to be less important. It is now thought that some infections such as bacteria, mycoplasma or viruses may cause the body’s immune system to misfire, causing the immune system to mistakenly view what it has as an enemy and attack itself, with the result that rheumatoid arthritis occurs. Another aspect is also the genetic issue of concern. There have been epidemiological surveys that show that the onset of rheumatoid arthritis is indeed closely related to genetics, and people with a family history of rheumatoid arthritis tend to be more prone to rheumatoid than others, and many studies have found that this is closely related to HLA-DR4, this gene. So, what are the chances that a child will develop rheumatoid arthritis when the patient has rheumatoid arthritis? The answer is 11%. In fact, the main pathogenesis currently recognized is immune disorders. C4+ T cells and MHC-II class antigen-presenting cells infiltrate the synovial membrane, initiating a specific immune response that leads to the development of synovial inflammation, resulting in the development of inflammation that can lead to joint swelling and pain, slowly destroying cartilage and bone, resulting in joint deformity. Thus, rheumatoid joint pathogenesis is very complex and environmental, genetic and immune disorder factors can all be involved, acting in combination, leading to the development of rheumatoid arthritis.