The literature supports that humoral autoimmunity against ApoA-1 is a rather frequent phenomenon associated with poorer clinical outcomes, disease activity, and subclinical atherosclerosis in various settings, including autoimmune diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematous (SLE), and cardiovascular (CV) diseases, and in the general population (1–4). This evidence concerns the gene APOA1 and rheumatoid arthritis.