This limit will acquire greater importance in the near future, because it is expected to equally hinder feasibility of all next-line targeted therapies for ALK+ NSCLC, for example also newly-developed fourth-generation ALK inhibitors directed against compound ALK mutations (30), or other drugs targeting other actionable resistance mechanisms, such as acquired MET amplifications or KRAS mutations (9). This evidence concerns the gene KRAS and non-small cell lung carcinoma.