In CRC, DDX5 and DDX17 formed complexes with β-catenin and augmented β-catenin to activate the transcription of proto-oncogenes, including c-Myc, cyclin D1, c-jun, and fra-1, and suppress the transcription of the cell cycle inhibitor p21(WAF1/CIP1), which is mediated via c-Myc, resulted in the promotion of CRC cell proliferation and tumor formation (22). This evidence concerns the gene JUN and colorectal carcinoma.