A constitutive activation of the RAS/ERK/MAPK signaling pathway is frequently driven by activating mutations in BRAF or NRAS.[26] Activating mutations in the BRAF oncogene are present in 50 to 60% of melanomas, 90% of which produce an active mutant BRAFV600E protein.[27–29] Recently developed BRAF inhibitors as well as immune checkpoint inhibitors can be highly effective in some patients leading to a tremendous survival gain in metastatic melanoma.[30, 31] However, a substantial proportion of patients either do not respond or develop therapy resistance.[32–35]. Here, NRAS is linked to melanoma.