This is supported by our previous data demonstrating that the xCT selective inhibitor, SASP, blocks PEL tumor progression in an immune-deficient xenograft model [5], suggesting that the infectious process of KSHV is directly linked to post-entry mechanisms involved in virus-associated lymphomagenesis, but the mechanisms by which xCT orchestrates this link are not fully defined. This evidence concerns the gene SLC7A11 and neoplasm.