Tyrosine kinase inhibitors (TKIs) are the standard of care treatment for oncogenic epidermal growth factor receptor (EGFR)-driven lung adenocarcinomas.1 Despite the efficacy of TKIs, responses are heterogeneous and drug resistance inevitably emerges, underscoring the need to identify determinants of therapeutic sensitivity.1 Understanding how genotypes influence responses to drugs could help advance treatment strategies for different subsets of patients with EGFR-driven lung cancer and delay or prevent the emergence of resistance. The gene discussed is EGFR; the disease is lung cancer.