NSCLC in nonsmokers tends to be driven by a single somatic mutation or a gene fusion[2], such as mutated epidermal growth factor receptor (EGFR)[3], v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS)[4], the echinoderm microtubule associated protein like 4 (EML4) and anaplastic lymphoma receptor tyrosine kinase (ALK) genes (EML4-ALK)[5], etc. These have been proven to be “driver” genes in some subgroups of lung cancers. This evidence concerns the gene EML4 and lung cancer.