HNSCC, which is known to have EMT characteristics, shows more vascular invasion and metastases, as well as a poorer prognosis.17, 18 It has been reported that CUL4B knockdown in NSCLC inhibits EMT progression and decreases the level of c‐myc, cyclin D1, and β‐catenin.19 In addition, CUL4B overexpression significantly enhanced the growth of hepatocytes in liver cells in a recently established mouse model.20 Here, we investigated whether CUL4B expression regulates EMT in HNSCC cells to determine whether CUL4B drives tumor proliferation. The gene discussed is MYC; the disease is neoplasm.