Transforming growth factor beta (TGF-β) plays a crucial role in tissue repair but can also contribute to disease when its activity is excessive. This review explores the dual role of TGF-β in tissue repair and disease, highlighting its involvement in fibrosis and scarring. TGF-β is a multifunctional cytokine that promotes healing by stimulating the production of extracellular matrix components, such as fibronectin, collagen, and proteoglycans. However, excessive TGF-β activity can lead to the formation of scar tissue and fibrosis, which can be detrimental in various diseases, including kidney disease, lung fibrosis, liver cirrhosis, and others. In kidney disease, TGF-β is implicated in the development of glomerulonephritis and diabetic nephropathy. Elevated TGF-β levels are associated with increased extracellular matrix deposition and fibrosis in the kidney. Inhibitors of TGF-β may offer therapeutic potential in controlling these conditions. TGF-β is also involved in fibrotic diseases of other organs, such as the lungs, liver, heart, and skin. Its role in scarring is particularly interesting, as it is known that fetal skin heals without scarring, but post-birth healing leads to scarring, suggesting that TGF-β is involved in this process. TGF-β also has immunosuppressive properties, which may be beneficial in autoimmune diseases and in the context of AIDS. However, its excessive activity can contribute to immunosuppression and disease progression. The complex regulation of TGF-β activity presents opportunities for therapeutic interventions, including the use of TGF-β inhibitors. These inhibitors have shown promise in reducing excessive extracellular matrix deposition without interfering with normal tissue healing. The development of more effective TGF-β inhibitors is an important area of research for the treatment of diseases caused by the "dark side" of TGF-β activity.Transforming growth factor beta (TGF-β) plays a crucial role in tissue repair but can also contribute to disease when its activity is excessive. This review explores the dual role of TGF-β in tissue repair and disease, highlighting its involvement in fibrosis and scarring. TGF-β is a multifunctional cytokine that promotes healing by stimulating the production of extracellular matrix components, such as fibronectin, collagen, and proteoglycans. However, excessive TGF-β activity can lead to the formation of scar tissue and fibrosis, which can be detrimental in various diseases, including kidney disease, lung fibrosis, liver cirrhosis, and others. In kidney disease, TGF-β is implicated in the development of glomerulonephritis and diabetic nephropathy. Elevated TGF-β levels are associated with increased extracellular matrix deposition and fibrosis in the kidney. Inhibitors of TGF-β may offer therapeutic potential in controlling these conditions. TGF-β is also involved in fibrotic diseases of other organs, such as the lungs, liver, heart, and skin. Its role in scarring is particularly interesting, as it is known that fetal skin heals without scarring, but post-birth healing leads to scarring, suggesting that TGF-β is involved in this process. TGF-β also has immunosuppressive properties, which may be beneficial in autoimmune diseases and in the context of AIDS. However, its excessive activity can contribute to immunosuppression and disease progression. The complex regulation of TGF-β activity presents opportunities for therapeutic interventions, including the use of TGF-β inhibitors. These inhibitors have shown promise in reducing excessive extracellular matrix deposition without interfering with normal tissue healing. The development of more effective TGF-β inhibitors is an important area of research for the treatment of diseases caused by the "dark side" of TGF-β activity.