Previously, we reported that in AXL-high-expressing EGFR-mutated NSCLC, a small population of tumor cells emerged tolerant to osimertinib as persisters by restoring the survival signal from AXL associated with EGFR and HER3, and the combined treatment with osimertinib and an AXL inhibitor prevented the development of acquired resistance to osimertinib12. The gene discussed is AXL; the disease is non-small cell lung carcinoma.