It has been reported that putative vasohibin 2 (VASH2) abnormally overexpresses to promote HCC proliferation and inhibits apoptosis, which resulted from the lower H3K27 trimethylation, and higher high H3K4 trimethylation and H3 acetylation at VASH2 promoters (74). This evidence concerns the gene VASH2 and hepatocellular carcinoma.