40. In addition, it has been found that BIK can be induced to increase cell cancer apoptosis, and these regulatory mechanisms may serve as important targets for tumor therapy drugs 41. However, the mechanism by which BIK expression is inhibited is unclear. Our results demonstrated that knockdown of LINC00662 could induce the expression of BIK by EZH2-dependent manner. Many lncRNAs regulate the level of H3K27me3 of specific gene promoter loci via recruiting and binding to EZH2, and EZH2-mediated epigenetically regulation plays a crucial role in process of tumor development42. Here, LINC00662 is linked to neoplasm.