Upon mECK36 tumor formation in mice, explanted cells that are forced to lose the viral episome continue being tumorigenic [23]; in part and as we have recently shown, by the irreversible in vivo acquisition of host mutations, as the PDGFRA activating mutation D842V, the most common PDGFRA mutation in GIST, which confers constitutive RTK activity and resistance to Imatinib, supporting the ideas that: 1) PDGFRA is an oncogenic driver in KSHV tumors and 2) Oncogenic mutations may compensate for the loss of KSHV driving tumorigenesis in the absence of the virus [22]. This evidence concerns the gene PDGFRA and Kaposi's sarcoma.