Taken together, the data presented here identify the mechanism through which HIV-1 vp17s can promote B-cell proliferation, suggesting that, from a therapeutic point of view, new strategies that exploit drugs targeting PAR1, EGFR, HER2, and MMPs, might prove useful to inhibit the growth-promoting and clonogenic activity of vp17s and therefore contributing to a more effective treatment of HIV-related lymphomas and other cancers associated with HIV- infection. This evidence concerns the gene EGFR and lymphoma.