RAS mutations result in the constitutive activation of the MAPK pathway, leading to uncontrolled cell proliferation and resistance to apoptosis-inducing drugs.2,3 Although many RAS inhibitors have been isolated and studied, the development of drugs targeting RAS is limited by a lack of well-defined druggable nooks and cavities on the RAS surface.4 However, interrupting signals between RAS and downstream effectors, such as the RAF–MAPK kinase (MEK)–extracellular signal-related kinase (ERK) pathway, could represent a new therapeutic strategy for RAS-driven cancers.5–7. The gene discussed is RAF1; the disease is cancer.