The key finding of our present study is represented by the identification of a new chain of kinase reaction in glioma cells, activated by upregulated SPHK1, sequentially causing phosphorylated activation of Akt, phosphorylated inactivation of FOXO3a and downregulation of Bim, and consequently leading to evasion of glioma cells from programmed cell death or abrogation of chemotherapeutic agents-induced apoptosis. The gene discussed is FOXO3; the disease is glioma.