TGFB1 and congenital rubella syndrome: Recent studies highlighted novel molecular mechanisms of CRS, such as inflammation and activated oxidative stress (36, 37), TGF-β1/Smad signaling pathway (38, 39), Wnt/β-catenin signaling pathway (40, 41), hyperactive renin–angiotensin–aldosterone system (RAAS) (42, 43), dysbiosis of the gut microbiota (44, 45), and dysregulation of non-coding RNAs (46, 47).