Beta-glucuronidase (GUSB) activity has been found to be secondarily increased in tissues from MPS VI cats as result of ARSB deficiency.53 As further therapeutic endpoint, GUSB activity was thus evaluated in tissues of MPS VI mice treated with either the combination of 6 × 1011 gc/kg of AAV and ERT or single therapies, and in NR and AF controls. The gene discussed is ARSB; the disease is atrial fibrillation.