Furthermore, when METex14 was expressed in normal mouse NIH3T3 fibroblasts, cells were transformed and then became tumorigenic in vivo, which confirmed METex14 as a driver alteration [17], whereas Paik and colleagues were demonstrating METex14 tumor cells were sensitive to MET tyrosine kinase inhibitors (TKIs), and the clinical benefit for NSCLC patients was demonstrated [18]. The gene discussed is MET; the disease is neoplasm.