CLK3 was found to be upregulated in cholangiocarcinoma (CCA) patients and plays a role in nucleotide metabolism.124 Meanwhile, a gain of function somatic mutation Q607R was identified in CLK3 kinase domain, which induced USP13 Y708 phosphorylation and promoted USP13 binding to c-Myc. This evidence concerns the gene MYC and cholangiocarcinoma.