The association of aCL and anti-NPM antibodies in WB lupus-prone mice and patients with SLE might be explained by two different mechanisms: first, cross-reactivity due to the expression of a shared epitope by CL and NPM, or second, the ability of NPM to interact with CL to form an immunogenic complex able to induce the two antibody populations and/or a unique antibody population able to react with both NPM and CL (dual reactivity), as reported for lupus-related antigen particles [22-24]. This evidence concerns the gene NPM1 and systemic lupus erythematosus.