However, no matter whether KSR proteins represent real pseudokinases or reactivate residual intrinsic kinase activity under certain circumstances promoting a catalytically competent kinase domain fold, there is clear biochemical and genetic evidence that truly kinase-dead cancer-associated BRAF mutants, such as BRAFD594G lacking the catalytic aspartate of the DFG-motif, activate the MEK/ERK pathway by acting as dimerization partners of catalytically competent RAF proteins [104,105]. Here, BRAF is linked to cancer.