Notably, essentially the same response to eIF4Fi was observed in NRAS-mutant lines (MelJuso, SkMel30; Fig. 5B), indicating that the strong upregulation of c-Fos and EGR1 transcription factors could be a universal response of human melanoma cells to eIF4Fi, potentially also contributing to their survival under the conditions of inhibited eIF4F activity. Here, NRAS is linked to melanoma.