Recently, by using vemurafenib-resistant melanoma cells as a target of the selection and sensitive cells in counter-selection steps, Li et al. identified an aptamer specifically binding to CD63 on the surface of cancer cells [72], thus opening the possibility to interfere with the TIMP-1/CD63 interaction at the cell surface, which recently emerged as a driver of malignant progression in melanoma and other human cancers [73]. This evidence concerns the gene CD63 and melanoma.