Fibrosis is pointedout to trigger renal I/R injury and is themain mechanism associated with the development of chronic kidney disease(CKD). We have previously demonstratedthat immunostaining of renal tissue derived from the I/R model ispositive for TGF-β1 and fibronectin and associated with an augmentedcollagen deposit., Cortes et al. also demonstrated the augmentation of MMP-9 activity andprotein content in the renal cortex of I/R rats, which is similarto our finding. The gene discussed is TGFB1; the disease is chronic kidney disease.