The MAP kinase pathway is activated by ligand binding to a transmembrane receptor, which switches Ras on via GEF (Guanine nucleotide Exchange Factor) that counteracts GAP (GTPase Activating Protein) activity. Ras-GTP in turn activates the downstream signaling intermediates (kinases), which are activated by sequential phosphorylation. Which drug CANNOT be used to target cancer cells that have elevated receptor activation

The mitogen-activated protein kinase (MAPK) is a pathway composed of proteins that amplify and integrate signals from receptors localized on the surface of cells and trigger the transcription of specific genes in the nucleus of the cell. In eukaryotic organisms, the MAPK pathway is known to control critical cellular processes such as, for example, cell proliferation, cell differentiation, cell death, etc. RAS proteins are GTPases localized to the plasma membrane involved in MAPK signaling. Moreover, the GTPase activating proteins such as RasGAP (Ras GTPase activating protein) regulate Ras-GTP bound by promoting GTP hydrolysis. It has been shown that RasGAP expression is down-regulated in different types of cancer. In this regard, it has been proposed that the interference of GAP activity should result in an enhanced Ras protein activation in cancer cells, thereby initiating tumorigenesis by inducing, for example, uncontrolled cell proliferation.