Tracking MET de-addiction in lung cancer: a road towards the oncogenic target.

Lung cancer is the most common cause of cancer-related mortality worldwide and adenocarcinoma represents its most common histological subtype[1]. With the advent of targeted therapy, the outcome of those lung cancer patients harboring somatically activated oncogenes, such as the mutant epidermal growth factor receptor (EGFR) or the translocated anaplastic lymphoma kinase (ALK), has considerably improved over the last decade[2]. Pivotal genomic studies have been performed in order to broaden the landscape of targetable alterations[3,4].

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