Infection with KSHV has been reported to contribute to neoangiogenesis, another characteristic feature of KS lesions, by upregulating the expression of several genes involved in the control of vascular modeling and angiogenesis, such as VEGF-A, VEGF-C, angiopoietin-related protein 4, thrombomodulin, and matrix metalloproteinase (MMP-1) [32]. This evidence concerns the gene VEGFC and infection.