Recent research has suggested that the reflux of pancreatic enzymes into the bile duct and the gallbladder is an abnormal phenomenon that plays a role in lithogenesis and carcinogenesis by damaging the gallbladder epithelium and inducing molecular changes and mutations. [1][2][3][4][5][6] Pancreatobiliary reflux associated with pancreatobiliary maljunction (PBM) outside the duodenal wall is a well-known congenital anomaly and has been related to gallbladder mucosal damage, inflammation, and carcinogenesis. 6,7 It has also been suggested that among the causes of this abnormal reflux in patients with normal pancreatobiliary junction is the sphincter of Oddi (SO) dysfunction. [1][2][3] The biliary tract does not have peristalsis and consequently does not exert pressure on its intraluminal content; consequently, the pressure of the common bile duct depends exclusively on the function of the SO and