Melanoma genome sequencing and exome sequencing of an astonishingly high heterogeneity of clinical samples have led to the identification of a large catalog of recurrent somatic variants [2], most notably BRAF and NRAS. However, patient outcomes from treatment with novel compounds are compromised by an almost 100% recurrence rate due to rapidly occurring drug resistance [3] and melanoma suppression remains unpredictable when targeting protein-coding genes identified in large cohort sequencing projects. The gene discussed is NRAS; the disease is melanoma.