Selective targeting of the alternative pathway in lupus-prone mice with a recombinant CR2-fH chimera, which targets fH to tissue sites of C3 activation through CR2 binding, likewise reduced the production of anti-dsDNA and circulating ICs, increased serum C3 levels, and prevented the development of albuminuria and glomerular deposition of IgG, C1q, and C3 [30]. The gene discussed is C3; the disease is systemic lupus erythematosus.