Pathway analysis of transcripts in patient-derived BRAF mutant Mel 14-108 melanoma showed similar enrichment of pathways associated with cytokine–cytokine receptor interaction, ECM receptor interaction, and neuroactive ligand receptor interaction as in BRAF mutant M14 and A2058 models, whereas pathways distinct from those regulated by mutant BRAF, viz., cell cycle, DNA replication, Fanconi anemia, and DNA repair pathways, were enriched in patient-derived wild-type BRAF Mel 14-089 melanoma cells (Table S2). This evidence concerns the gene BRAF and Fanconi anemia.