Based on the findings, co-presence HPV/EBV infection or mono-infection is probably can contribute to these changes (i.e., E-cadherin, N-cadherin, Twist, PTPN13, Slug, CD44, Bcl-2, and Survivin), but further experimental studies are needed to prove the role of viral infections in the regulation of Anoikis molecular pathways and metastasis in PCa [73–78]. The gene discussed is SNAI2; the disease is Epstein-Barr virus infection.