Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of multiple autoantibodies in the body. For patients who are first diagnosed or whose diagnosis is unclear, doctors will usually screen for autoantibodies (mainly antinuclear antibodies ANA) and use it as one of the bases for judgment. So, does a positive autoantibody (ANA) necessarily mean SLE? The rate of positive antinuclear antibodies (ANA) in SLE patients is greater than 90%, and new studies have found that ANA and other antibodies can be detected up to 10 years before the appearance of clinical symptoms, which can be of great help in the early diagnosis of SLE. However, testing for these autoantibodies alone is not an accurate predictor of disease, as it is possible for normal individuals, but not SLE patients, to be positive for ANA. Epidemiologically, ANA(+) is predominantly associated with women at about 40-60 years of age, with a peak at 40-49 years of age, and high levels of ANA(+) are mainly confined to women. 80-90% of patients with SLE are women. This shows that the presence of autoantibodies, especially in women, has a tendency to develop into SLE. The majority of women with ANA(+) do not develop SLE throughout their lifetime, suggesting from the side that anti-nuclear autoimmune reactions outside of SLE disease have the potential to provide a beneficial immune response in women. In addition to ANA, other types of autoantibodies are found in normal individuals, with anti-SSA and anti-SSB antibodies appearing before clinical symptoms (mean 3.4 years) and SLE-specific anti-double-stranded DNA (dsDNA) antibodies appearing closer to the time of diagnosis (mean 1.2 years). Because ANA antibodies are more prevalent, these antibodies are more positive in women than in men, about 4:1. So why do autoantibodies appear in normal individuals? Does the long-term accumulation of different antibodies develop into an autoimmune disease? Studies have found that many factors can induce autoantibodies in the body, such as estrogen, smoking, drugs, environment, light exposure, occupational hazards such as pesticides or solvents, and viral infections. In addition, VitD deficiency has been associated with autoimmune abnormalities. Indeed, many people exposed to these risk factors do not eventually develop SLE, and underlying susceptibility, including risk factors such as gender and genetics, may require not only autoantibody production but also a transition from benign preclinical auto-reactivity to clinical autoimmune disease. In some cases, the boundary of clinical disease is due to an amplification of the immune process leading to irreversible organ damage. In contrast, SLE may have led to irreversible organ damage before the diagnosis is confirmed. Therefore, those who visit the doctor with positive autoantibodies on examination should not be overly nervous and anxious, but they should not be paralyzed and take a chance. They should consult a professional rheumatologist to make a comprehensive judgment of its clinical significance and follow professional advice before taking the next step.