In this study, we found that (1) LINC00470 is a positive regulator of AKT activation and it inhibited the nuclear translocation of phosphorylated AKT; (2) LINC00470 directly bound FUS and anchored FUS in the cytoplasm, resulting in FUS activation; (3) LINC00470 interacted with FUS and AKT to form a stable complex; and (4) LINC00470 decreased the ubiquitination of HK1, which affected glycolysis by positively regulating AKT activation in GBM tumorigenesis. This evidence concerns the gene AKT1 and glioblastoma.