Although no small molecular inhibitors that target RAF/RAF dimer interface have been developed at present, several groups have demonstrated that disrupting RAF/RAF dimers by using peptide inhibitors can effectively block hyperactive ERK signaling and thereby inhibit the growth of cancer cells harboring active RAF or RAS mutations[177-179], indicating that the RAF/RAF dimer interface is indeed a valid target for drug development. The gene discussed is RAF1; the disease is cancer.