In our recent report [33], we screened the deregulated signaling in the surgical tissues of CCA patients and found the activities and/or expression of several oncogenic molecules downstream of RTKs including hydrogen peroxide clone5 (Hic-5), known to be a critical mediator of hepatocellular carcinoma (HCC) progression [34,35]; Src, one of the nonreceptor tyrosine kinase; AKT, the serine threonine kinase downstream of PI3K; and JNK, one of the MAPK, elevated in tissues of a significant portion (about 40–50%) of metastatic CCAs. This evidence concerns the gene AKT1 and cholangiocarcinoma.