Key endpoints should include persistent HPV/EBV infection, relevant cytokine alterations (e.g., IL-10, TGF-β), and the development of colorectal precursors such as adenomas or dysplasia[15,17,25]. Combined with advanced molecular assays (e.g., E6/E7 mRNA expression, metagenomics), such studies could illuminate the causal pathways linking viral colonization to malignant transformation. This evidence concerns the gene IL10 and dysplasia.