By virtue of their ability to induce cell cycle arrest in G2/M by targeting PLK1 (ref. 19), and to dampen the DNA repair response through the inhibition of CHK2 activity, allosteric RAF inhibitors such as KG5 would be expected to have a broad application for the sensitization of genetically diverse tumours to the effects of cancer therapies such as ionizing radiation or etoposide that function by inducing genotoxic stress. This evidence concerns the gene RAF1 and neoplasm.