AT II is crucially involved in the manifestations of renal fibrosis by induction of pro-fibrotic effector molecules and EMT resulting in enhanced ECM production[138], and inhibition of AT II using angiotensin-converting enzyme (ACE) inhibitors or blocking agents towards the AT I receptor has emerged as a therapeutic approach to slow down renal disease progression[139] and revealed anti-fibrotic actions in the lung, heart and liver[140-143]. This evidence concerns the gene ACE and renal fibrosis.