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Upon ligand binding, c-Met homodimerizes and becomes phosphorylated. This leads to the recruitment of effector molecules such as Grb2, SHC, CRK/CRKL, PI3K, PLCγ, SRC, SHP2 and STAT3. These effector molecules in turn activate numerous signaling pathways both directly or indirectly. Notable examples include activation of RAS through the guanine nucleotide exchange factor SOS, AKT phosphorylation through PI3K, and STAT3 dimerization and translocation to the nucleus.