The identification of differentially abundant proteins—such as the upregulation of mitochondrial dicarboxylate carrier and hemopexin and the downregulation of osteocalcin, apolipoproteins (ApoA1 and ApoA-IV), and CCDC124—reflects the complex interplay between metabolic dysfunction, immune cell dysregulation, impaired bone remodeling, and defective apoptotic pathways in RA pathophysiology. This evidence concerns the gene APOA4 and rheumatoid arthritis.