The following explanations have been suggested: viral reactivation due to immunosuppressive therapy and chronic immunologic reaction between altered lymphoid cells and normal lymphocytes; in fact, HHV-8 infects both lymphatic and blood vascular endothelial cells and seems to target immunosuppressor tumor proteins (retinoblastoma and p53) causing the production of lymphangiogenic growth factors, (bFGF, Scatter factor, IL6, etc), endothelial cell proliferation, and tumorigenesis [12, 13]. This evidence concerns the gene TP53 and neoplasm.