With regards to EGFR-targeted agents, exon 19 deletions and exon 21 L858R substitutions, termed classic mutations, represent the most common genetic alterations, accounting for approximately 90% mutations in NSCLC adenocarcinomas and resulting in a high sensitivity to the first generation of EGFR-TKIs [1]. The gene discussed is EGFR; the disease is adenocarcinoma.