BRAF and cancer: Although the components of MAPK signaling do not assemble a super complex in BRAF-mutated cancer cells, constitutively active BRAF mutant still functions as homo- or hetero-dimers (BRAF/BRAF or BRAF/KSR) that can be disrupted by AMPK-driven phosphorylation of both N- and C-terminal 14-3-3 binding sites [230, 231, 233].