RA is an autoimmune disease that primarily impacts joints throughout the body. The disease can result in pain, stiffness, and reduced mobility. It is a chronic disease, meaning that it lasts a long time and can worsen over time if left untreated. As the disease progresses, it can lead to joint deformity and severe pain, which can significantly impact the patient's daily life. While there are treatments available to manage the symptoms of RA, there is currently no cure for the condition. Glucose-6-phosphate isomerase (GPI) is an enzyme that plays a key role in glycolysis, the metabolic pathway that breaks down glucose to produce energy. Establishment of two GPI-dependent arthritis mouse models (K/BxN and GPI protein-induced arthritis mouse models), successfully identifying GPI as one of the RA-associated autoantigens. In human RA, elevated levels of free GPI protein and anti-GPI autoantibodies were found in the sera and synovial fluid of RA patients. Despite extensive research on the pathogenicity of GPI in RA, many questions remain unanswered, including what are the major pathogenic B-cell epitopes of GPI? What is the prevalence of anti-GPI antibodies in RA patients? Are anti-GPI antibodies specific for RA disease? Cartilage Oligomeric Matrix Protein (COMP) is a glycoprotein that helps in the formation and maintenance of cartilage. It exists in the synovial fluid and serum of RA patients and the level of COMP have been found to be positively correlated with the severity of the disease. Studies have indicated that COMP might contribute to the breakdown of cartilage in RA by stimulating the production of inflammatory cytokines and activating enzymes known as matrix metalloproteinases. Anti-citrullinated protein antibodies (ACPAs) are autoantibodies that have highest specificity for RA. During the autoimmune stage of RA, which occurs years before clinical symptoms appear, the immune system already begins to produce ACPAs. Studies have shown that the production of ACPAs is highly associated with the HLA-DRB1*0401 ...