Previous studies demonstrated that to promote apoptosis, activated GSK3 could inhibit the interaction between VDAC and HK2.40,41 These findings uncover a previously unknown mechanism of c-Myc upregulation by LMP1 and identify a PI3-K/Akt-GSK3beta-FBW7-c-Myc signaling axis that enhances glycolysis in the presence of LMP1 in NPC cells. This evidence concerns the gene GSK3B and nasopharyngeal carcinoma.