We have previously shown that crossing the full-length (32 to 151 Mb) NZB c4 interval onto the lupus-prone B6.NZBc1 background leads to suppression of autoantibody production and renal disease, and have provided evidence through adoptive transfer experiments that this was mediated by a suppressive effect of NZB c4 CD5+ B cells [6,7]. The gene discussed is CD5; the disease is kidney disorder.