MET and lung cancer: Thus, we are far from fully understanding how SNXs work with the retromer.21–23 Irrespective of their association with the retromer, both SNX1 and SNX2 can interact with membrane receptors and modulate their recycling and degradation, including that of many G-protein-coupled receptors24–28 and receptor tyrosine kinases (RTKs), such as the hepatocyte growth factor (HGF)/Met receptor.14,29–33 Specifically, SNX2 interacts with Met and its depletion in lung cancer cells overexpressing constitutively active Met promotes its lysosomal degradation.34