Given the pro- and antitumorigenic effects of TGF-β in tumor progression (38, 39), further studies are needed to elucidate whether the KSHV-CD109 interaction represents an additional mechanism by which KSHV regulates TGF-β signaling during infection and KS development, particularly in the context of cellular senescence and aging. This evidence concerns the gene TGFB1 and Kaposi's sarcoma.