Akt seems to be essential in phosphorylating FOXO3a in current study because our results showed activation of Akt and Ser253 phosphorylation of FOXO3a in SPHK1-overexpressing glioma cells, as well as Akt inactivation and Ser253 dephosphorylation of FOXO3a in SPHK1-downregulated glioma cells. This evidence concerns the gene SPHK1 and central nervous system cancer.