This was based on the following lines of evidence: (1) LINC00470 was upregulated in GBM and its expression was positively correlated with p-AKT; (2) ectopic expression of LINC00470 or knockdown of LINC00470 increased or suppressed AKT activity and tumor cell proliferation, respectively; and (3) re-expression of LINC00470 in LINC00470-KO cells was able to restore AKT activation. Here, AKT1 is linked to glioblastoma.