On the other side, Nolan et al. have recently reviewed the kinase-independent functions of C-Raf and explored targeting its effectors, in particular proapoptotic proteins ASK1 and MST2, and suggested that disruption of these protein–protein interactions or design of kinase activators in the context of ASK1 or MST2 activation might be a new avenue for anti-RAS cancer therapy [88]. This evidence concerns the gene RAF1 and cancer.