In any case, disputing the involvement of angiogenic factors in STS, the principal mechanism proposed is that FGF-2 could recruit endothelial cells and increase the release of MMPs and uPa leading to extracellular matrix degradation and permitting tumour motility, vascular smooth muscle cells recruitment trough PDGF and pericytes coverage of newly formed vessels [55]. This evidence concerns the gene FGF2 and telomere syndrome.