Friedlaender A, Drilon A, Banna GL, et al. - In patients with non–small cell lung cancer (NSCLC), a continuous rise in clinically relevant driver mutations has been seen over the years, and, due to the development of effective treatments, dysregulated activation of the MET tyrosine kinase receptor has acquired significance among these. Researchers undertook this review to address the biology of MET. They focused on the diagnosis of clinically relevant alterations and their growing clinical importance, taking into account the development of multiple targeted therapies, both within the context of MET as a driver of resistance and on its own. They found that via various mechanisms, including gene amplification, overexpression of the receptor and/or its ligand hepatocyte growth factor, and the acquisition of activating mutations, MET dysregulation can originate. Nearly 3% to 5% of patients with NSCLC, predominantly adenocarcinoma, were found to carry MET mutations. MET mutations were found to be overrepresented in the sarcomatoid subtype. In 1% to 5% of NSCLC cases, also mainly in adenocarcinoma, de novo MET amplifications were evident.