An N-ethyl-N-nitrosourea (ENU)-generated uromodulin mutant [Ala227Thr (A227T)] mouse has been described to develop azotemia, impaired urine concentrating ability and reduced excretion of uric acid, but not renal fibrosis (Kemter et al., 2009), whilst a second ENU mutant, Cys93Phe (C93F), developed renal failure, urinary concentrating defects, interstitial fibrosis, inflammation and tubular defects (Kemter et al., 2013) (Table S1). The gene discussed is UMOD; the disease is kidney failure.