Each subtype shows a peculiar molecular background.2 EBV-associated neoplasms usually have the cyclin-dependent kinase inhibitor 2A gene (CDKN2A) silencing, the programmed death-ligand 1 (PD-L1) overexpression and mutations in phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA). Here, PIK3CA is linked to neoplasm.