Beside elevated expression of AngII in CCA tissues as well as high AT-I receptor immunoreactivity in both epithelial and stromal cells, AngII induced survival of iCCA cells as well as an increase in HSC activation (LI90), indicating a role for the AngII-AT-1 axis as a regulator of tumor progression, both in an autocrine and paracrine fashion. This evidence concerns the gene AGT and neoplasm.