In a murine lupus model, it has been shown that CTLA4-Ig, a recombinant fusion protein comprising a Fc fragment of human IgG1 which binds either to CD80 or CD86 with a much higher avidity than CD28, contracted the autoreactive B-cell population and reduced autoantibody production and Ig class switching [39]. The gene discussed is CTLA4; the disease is systemic lupus erythematosus.