The anti-apoptotic activities of EBV-encoded molecules, together with their ability to interfere with cell cycle regulators, may promote the outgrowth of immune and/or epithelial cells and the development of EBV-driven malignancies, such as BL, HL, DLBCL, LC, GC, NPC, NKTL, and AR-PCNSL. This evidence concerns the gene SCYL1 and laryngotracheoesophageal cleft.