This was in accordance with the report of Tao and colleagues, who have found that EZH2 overexpression inhibited miR‐181b expression, which directly targeted binding site of hexokinase 2 within the 3′‐UTR, thus inducing glycolysis and promoting progression in prostate cancer cells.40 Our results indicated that EZH2 overexpression might manipulate the migrative and invasive abilities through contributing to the tumour glycolysis of OSCC cells. The gene discussed is EZH2; the disease is neoplasm.