As shown in the B16 melanoma model, selective GSH depletion in tumor cells can be achieved by combining in vivo administration of G3139 [increases GSH efflux through cystic fibrosis transmembrane conductance regulator (CFTR); a multidrug resistance protein 1 (MRP1)-like member of the ABC family of transport proteins], verapamil (VRP, accelerates the loss of GSH by activation of MRP1), and acivicin [ACV, blocks γ-glutamyl transpeptidase (γ-GT) and prevents recycling of L-cysteine from the extracellular pool of GSH] [11]. Here, CFTR is linked to neoplasm.