The RAS protein functions as a molecular switch due to the activities of RAS-GEFs and RAS-GAPs. The GAP induces RAS to hydrolyze its bound GTP more rapidly than it would without this encouragement. Consider a mutant cell that expresses RAS-GAP at a much higher level than wild-type cells. Predict the response of mutant cells to extracellular signals that activate Receptor Tyrosine Kinase signaling.