Background: In advanced biliary atresia, the majority of TGF-hepatic expression is restricted to hepatocytes. These results imply paracrine fibrogenesis-driven by TGF-β1 in advanced biliary atresia. Objective: To study the hepatic expression of TGF-β1 in biliary atresia (BA) as well as other causes of neonatal cholestasis. Patients and Methods: This study included sixty infants from those who attended to the Pediatric Hepatology Gastroenterology and Nutrition Department, National Liver Institute, Menoufia University from September 2019 to May 2021. They were divided into two groups: Group 1 (biliary atresia group): included 30 infants diagnosed as biliary atresia patients that was subdivided into 2 sub-groups, successful Kasai group (14) and failed Kasai group (16). Group 2 (non-biliary atresia cholestatic group): included 30 infants with other causes of neonatal cholestasis as control group. Results: Patients with BA were easily distinguished from those with other infantile cholestatic liver disorders using the BA scoring system (98.83 percent). There was significant difference between the successful and failed Kasai groups regarding postoperative complication, recurrent cholangitis, surgical outcome at (three months, six months, one year, two years postoperatively), (P <0.05). Hepatic TGF Beta1 expression (in both biliary epithelial cells and liver cells) differed significantly between the non-atresia cholestatic group and both BA subgroups (P <0.01). Conclusions: Intraoperative cholangiography (IOC) verified the diagnosis of BA in surgical patients who were promptly referred for treatment. Hepatic expression of TGF Beta1 (biliary epithelial cells and liver cell expression) was significantly different between the non-atresia cholestatic group and biliary atresia subgroups.