3p and 9p which harbor the TGFBR2 and CDKN2A loci, respectively, are consistently found in precancerous lesions of NPC, pointing to a central role for CDKN2A loss and impaired TGF-β signaling in creating a susceptible NPE cell population capable of supporting EBV latency during early cancer development1,2,29–31. The gene discussed is CDKN2A; the disease is cancer.