Differentiation of B lymphocytes into plasma cells and increased immunoglobulin secretion may turn into autoantibody production and contribute to the pathogenesis of SLE, with increased levels of cytokines playing complementary roles, such as IL-4 cytokine promoting B cell differentiation into auto-antibody producing cells, IL-13 maintaining B cell survival, and IL-5 supporting eosinophil survival and tissue inflammation. This evidence concerns the gene IL4 and systemic lupus erythematosus.