Although targeting Notch signaling might be effective in treating CCAs, the adverse effects on the gastrointestinal tract [37, 38] are problematic; therefore, ASPH may be a more specific target to alter Notch activity since MO-I-1151 significantly inhibits CCA cell proliferation, migration, invasion, colony formation and CSC generated spheroids by inhibition of its β-hydroxylase activity, which is more potent and efficient than DAPT. Here, ASPH is linked to cholangiocarcinoma.