We also showed, through the robust upregulation of the expression of KDR and FLT4 in L1T2 versus TIVE cells, that L1T2-derived mouse xenografts could be a model for studying pathways, such as VEGF activation in KSHV infection and neoplasia, but they cannot be used to resolve the endothelial origin of KS, as they lack appropriate lineage markers. This evidence concerns the gene KDR and neoplasm.