Environmental and genetic factors influence lung cancer pathogenesis with cigarette smoke being the major environmental risk factor and a growing number of genetic alterations (including activating mutations in EGFR—Epidermal growth factor receptor, cMET—Hepatocyte growth factor receptor transmembrane tyrosine kinase pathway, ALK—Anaplastic lymphoma receptor tyrosine kinase and ROS-1—ROS proto-oncogene 1, receptor tyrosine kinase) being recognized as the driving forces underlying lung cancer development in non-smokers [2,3]. Here, ALK is linked to lung cancer.