Fibrosis development is mainly dependent on the humoral disbalance between oxidative load, pro-proteosynthetic, and pro-proliferative factors such as angiotensin II, aldosterone, endothelin, or catecholamines on the one side and substances with growth attenuating potential, such as nitric oxide (NO), prostacyclin, or atrial natriuretic peptide [54–56] on the other side. This evidence concerns the gene AGT and fibrosis.