Mice that lacked sFasL (mFasL intact) appeared normal, while mice lacking mFasL (sFasL intact) had higher NF-kappaB activation and developed a lupus-like autoimmune kidney disease more severe than gld/gld mice (which lack sFasL and mFasL) [70]. The gene discussed is FASLG; the disease is systemic lupus erythematosus.