Previous studies have focused on the involvement of TIMP3 in kidney pathology (Kassiri et al, 2009; Kawamoto et al, 2006): loss of TIMP3 associated with renal fibrosis and tubular interstitial injury in a mouse model of unilateral urethral obstruction (UUO; Kassiri et al, 2009), even though in human kidney biopsies TIMP3 expression was shown to be increased in patients with diabetic nephropathy secondary to T2DM or with chronic allograft nephropathy compared to healthy controls, possibly as a compensatory mechanism aimed at minimizing renal damage and disease progression. The gene discussed is TIMP3; the disease is diabetic kidney disease.