The patients of lung adenocarcinoma with EGFR mutations have a better response to EGFR tyrosine kinase inhibitors (TKIs) than those without EGFR mutations, while patients that are ALK-positive show a better response to the TKI crizotinib, suggesting that therapeutic effectiveness can be linked to the presence of specific driver mutations [10–13]. The gene discussed is ALK; the disease is lung adenocarcinoma.