To explore whether MANF is also a biotherapeutic protein for ADTKD caused by other UMOD mutations, we utilized UmodC147W/+ mice9, which harbor a human UMOD missense mutation and develop CKD and renal fibrosis more slowly than our deletion mutation mice. The gene discussed is MANF; the disease is autosomal dominant medullary cystic kidney disease with or without hyperuricemia.