Subsequent identification of ALK rearrangements [50] and several cancer‐driver events, including ROS1, NRG1, NTRK1/RET fusion, BRAF (V600E) mutation, or MET amplification/Exon14 skipping, strengthened the concept of oncogene addiction and tumor heterogeneity as a pillar of modern cancer therapeutics [49]. This evidence concerns the gene ALK and cancer.