SSAs exert their biological actions by binding to a family of G protein-coupled, seven transmembrane-spanning somatostatin receptors (sst1-sst5) in neuroendocrine cells, which, depending on the tumor type and the specific set of receptors involved, lead to decreased hormonal secretion, decreased growth and mitotic rates, increased apoptosis, and/or inhibition of cell signaling and protein synthesis, including inhibition of production and secretion of various angiogenic factors [8–11]. The gene discussed is SSTR1; the disease is neoplasm.