The large cytosolic C terminus of LMP1 provides docking sites for several signaling adapter proteins, which trigger various downstream oncogenic signaling pathways, such as the NF-κB, PI3-K/Akt and JAK/STAT pathways.6 In this way, LMP1 promotes malignant phenotypes, including resistance to apoptosis, and increased angiogenesis, invasion and metastasis in EBV-harboring cancer cells.7, 8, 9 However, the relationship between LMP1 and metabolic changes is still unclear. This evidence concerns the gene AKT1 and cancer.