Because: a) pazopanib is a potent chaperone inhibitor; b) the [pazopanib + AR42] drug combination has pre-clinical and clinical activity in sarcoma and renal carcinoma; and c) that B-RAF and RAF-1 rely on the chaperones HSP90 and HSP70 to maintain their active conformations, we performed studies in multiple PDX models of human melanoma, including vemurafenib resistant isolates, where cells expressed various mutated active forms of B-RAF. This evidence concerns the gene BRAF and melanoma.