Additionally, MALAT1, a non-coding RNA, transcriptionally activated through SYK/c-MYC pathway, enhanced the malignant traits of ES cells; however, its inhibitors suppressed cell viability and tumor formation in ES cells in vivo and in vitro via the inhibition of the AKT pathway (Figure 1; Sun et al., 2017). This evidence concerns the gene AKT1 and neoplasm.