EGFR activation via ERK1/2 enhanced focal adhesion turnover via FAK, leading to higher migration speed and fostering of CCA cell motility in addition to inhibiting FOXO4 via activation of PI3K/AKT signaling [50], suggesting the P13K/AKT/mTOR pathway, also reported for HB [11]. This evidence concerns the gene MAPK3 and cholangiocarcinoma.