Preclinical work in large NRAS‐mutant melanoma panels demonstrated that concurrent panRAF and MEK inhibition (e.g., Amgen compound A + trametinib) yields broad synergy, deeper pathway suppression, and apoptosis in MAPK‐dependent models; complementary functional screens implicate CRAF as a central bypass driver and show dual panRAF/MEK blockade can overcome diverse resistance mechanisms (Whittaker et al. 2015; Atefi et al. 2015). Here, NRAS is linked to melanoma.