Although BRAFV600E mutated melanomas, which represent 40–60% of this tumor entity, are effectively targetable with the BRAF inhibitor vemurafenib,1 relapse occurs as early as within approximately 5 months.2 Resistant tumors exhibit upregulation of receptor tyrosine kinase receptors PDGFRB3 or EGFR,4 signaling mediators such as CRAF or NRAS, as well as mutations in MEK1, MEK2 and NRAS resulting in the stimulation of the RAS/RAF/mitogen-activated protein kinase pathway (reviewed in Spagnolo et al.2). This evidence concerns the gene NRAS and melanoma.