CFTR and melanoma: As explained above, GSH efflux activation through MRP1 and a putative GSH transporter of an undefined molecular nature that was found to correspond to CFTR in B16 melanoma cells, limitation of Cys supply for de novo synthesis of GSH, and glutamate (Gln-derived)-induced competitive inhibition of cytosolic GSH transport into mitochondria, can promote both cytosolic and mitochondrial GSH depletion in the tumor cells.