MYC and neoplasm: In a proportion of these tumors, mutant BRAF may partly explain an overactivation of the Wnt-β-catenin-MYC axis which, along with dysregulated post-translational processes such as PIAS-mediated sumoylation, would contribute to a metabolic reprogramming characterized by enhanced glycolysis in tumor cells, gMDSC, and fibroblasts.