FOLH1 and cancer: 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)).