A variety of genes influences the development of EBV-related neoplasms and signaling pathways, which includes activation of oncogenes such as Bcl-2 and MYC, as well as signaling pathways including NF-B, JNK, JAK/STAT, and PI3K/Akt, and deactivate tumor suppressors such as p53, p27kip1, p21WAF1/CIP1, p16INK4A, p73, PRDM1, DICE1, and p27kip1(I, II) [14]. This evidence concerns the gene BCL2 and neoplasm.