EBV latent infection causes genomic instability through different mechanisms independently mediated by EBNA1 and EBNA3C, and LMP1 [36]; among these LMP1 inhibits DNA repair in epithelial cells through distinct mechanisms, including its ability to inhibit DNA-PK/AMPK signaling [37], to inhibit PI3K/Akt/FOXO3a signaling [38], and to downregulate expression of ATM. The gene discussed is PRKDC; the disease is disease arising from reactivation of latent virus.