The specificity of the SST-dependent anti-angiogenic effect, when compared to the direct anti-tumor activity was demonstrated, by the observation that it was, in most cases, independent of PTPs, but it involves the inhibition of cAMP accumulation [70] and, more importantly, the activity of endothelial nitric oxide synthase (eNOS) and the consequent generation of nitric oxide (NO) [69]. The gene discussed is NOS3; the disease is neoplasm.