To chemically probe the function of AXL in the context of collateral gefitinib resistance, we used YD (Fig. 7a), an antitumor agent we previously characterized to have concurrent AXL-dependent inhibitory mode-of-action in addition to having EGFR-targeting activity in gefitinib-resistant lung cancer models32,33. The gene discussed is EGFR; the disease is lung carcinoma.