As opposed to passive drug targeting, relying solely on the pathophysiological properties of target tissue, the active targeting exploits highly (over)-expressed receptors by (i) cancer cells themselves (e.g. epidermal growth factor receptor (EGFR), transferrin receptor, folate receptor, prostate-specific membrane antigen (PSMA) or glycoproteins) or (ii) tumor endothelial cells (e.g. VEGF receptors VEGFR1 and VEGFR2, αvβ3 integrins or matrix metalloproteinases (MMPs)). This evidence concerns the gene FOLH1 and neoplasm.