The high metastasis rate induced by MALAT1 is associated with agonism of the PI3K/AKT pathway and reduced E-cadherin expression via the involvement of EZH2.[63] Furthermore, MALAT1 can act as an miRNA sponge to regulate the miR-34a/cyclin D1 and miR-206/CDK9 axes, promoting OS tumor cell viability, proliferation, and activating tumor progression.[63,64]. The gene discussed is AKT1; the disease is neoplasm.