Genetic profiling of stage IV lung adenocarcinomas is state of the art to identify patients who are eligible to tyrosine kinase inhibitors targeting EGFR, and fused genes involving ALK, ROS and RET. Following the discovery of the oncogenic EML4-ALK fusion gene by Soda et al. [1], a series of trial data (phase I-III) published between 2010 and 2014 demonstrated the efficacy of crizotinib [2–4], a tyrosine kinase inhibitor that was originally developed to target MET [5] in non-small-cell lung cancer patients and led to rapid approval of the FDA and subsequently the EMA. Here, EML4 is linked to non-small cell lung carcinoma.