Finally, we demonstrate that adeno-associated virus (AAV) vector delivery of a homodimeric mini-FH (HDM-FH) molecule, previously shown to be efficacious in reducing glomerular C3 in FH-deficient mice (30), can significantly reduce glomerular C3 in our CFHR5 nephropathy mouse model and, thus, could be a future therapeutic approach for treating C3G associated with abnormal FHR proteins. The gene discussed is FH; the disease is Nephropathy.