In HCC, overexpression of EZH2 represses miR-622 through H3K27me3 deposition and results in CXCR4 upregulation and unfavorable prognosis, while BMI1 enhances TGFβ2/SMAD pathway and facilitates tumor cell proliferation and cell cycle progression [29, 30]. This evidence concerns the gene EZH2 and neoplasm.