Cdk5 phosphorylates the STAT3 transcription factor on its Ser-727 residue, leading to increased proliferation and promotion of tumor formation in medullar thyroid carcinoma and in prostate cancer cells through the activation of androgen receptor [3,4] or resistance to DNA-damaging agents through the increased transcription of the DNA-repair gene essential meiotic structure-specific endonuclease 1 (EME1) in colorectal cancer (CRC) cell lines [5]. The gene discussed is CDK5; the disease is neoplasm.