Tat increases the availability of soluble bFGF in the KS lesion, which promotes spindle and endothelial cell growth [32, 33] and up-regulates the receptors for fibronectin and vitronectin (integrins α5β1 and αvβ3 respectively), thus increasing the adhesion signals the cells require in order to grow in response to bFGF [34]. This evidence concerns the gene FGF2 and Kaposi's sarcoma.