“…It has been shown that the PBG and its proliferating Sox9 + progenitor cells [ 14 ] drive bile duct regeneration. The BDE is highly vulnerable to ischemia, and although minor lesions often lead to re-epithelialization, more severe injuries can result in fibrosis and stricture formation [ 4 , 15 ]. In general, injuries produced by ischemia (warm/cold ischemia, reperfusion injury, disturbed blood flow), immunological factors (ABO incompatibility, immune disease, virus infection, chronic rejection, chemokine mutations), or exposure to bile salts, can trigger post-transplant NAS cholangiopathies [ 16 ].…”