Due to the role of EGFR in promoting various cancers, including lung and oral cancer [33, 44], we can hypothesize that the mechanism used by vp17s, which involves the PAR1-triggered EGFR transactivation, might be also extended, in addition to aggressive B-cell NHLs, also to other AIDS-defining cancers, like Kaposi’s sarcoma and cervical cancer or to non-AIDS-defining cancers, as Hodgkin lymphoma or cancer of the oral cavity/pharynx, lung, anus and liver [45, 46]. This evidence concerns the gene F2R and Kaposi's sarcoma.