Though wildtype RAF inhibitors show limited anti-tumor activity in KRAS or BRAF mutant cancers in clinical trials, ATP-competitive RAF inhibitors that selectively target BRAF V600E monomers such as vemurafenib, dabrafenib and encorafenib increase clinical benefit, but they often paradoxically activate ERK signaling by transactivation of the other protomer in RAF dimers, which eventually results in drug resistance. The gene discussed is KRAS; the disease is neoplasm.