We quantified the impact of inactivating 10 putative tumor suppressor genes on the response to osimertinib within our mouse model and found that Kelch-like ECH associated protein 1 (Keap1) inactivation reduced sensitivity to this therapy.3 Our in vivo data mirror clinical data suggesting that KEAP1 pathway alterations predict poor clinical responses to TKIs.3 Thus, we established a causal link between this tumor suppressor pathway and TKI sensitivity in EGFR mutant lung adenocarcinoma. The gene discussed is EGFR; the disease is neoplasm.