AMPKi by pharmaceutical inhibitors abolishes the dimer-dependent paradoxical activation of MAPK signaling driven by the RAF inhibitors in Ras-mutated cancers, suggesting that AMPK-mediated phosphorylation of the C-terminal 14-3-3 binding site on CRAF promotes the intermolecular association of 14-3-3 dimers with CRAF homo- or hetero-dimers [231] (Fig. 4a). This evidence concerns the gene RAF1 and cancer.