Indirect mechanisms by which SSAs exert antiproliferative effects involve the inhibition of circulating growth factors such as insulin-growth factor (IGF), vascular endothelial growth factor (VEGF), growth hormone (GH), platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), as well as inhibition of tumor angiogenesis by inhibiting the proliferation and migration of endothelial cells and monocytes, which secrete proangiogenic factors [226–229]. This evidence concerns the gene GH1 and neoplasm.