Further relevant drug resistance mechanisms in BRAF-mutant cancers include phenotype switching (MITF/WNT5 pathways), immunomodulation and changes in the tumor microenvironment, metabolic rewiring (glucose, glutamine, lipid and mitochondrial metabolisms), and epigenetic modifications (histone and DNA modifications, non-coding RNAs)[7]. The gene discussed is BRAF; the disease is neoplasm.