In the absence of osimertinib treatment, RBM10 KD did not initiate tumor formation in noncancerous Beas2B human bronchial epithelial cells lacking canonical driver mutations (Supplemental Figure 3A), nor did RBM10 KD significantly enhance tumor growth or proliferation in H3255 or PC-9 patient-derived EGFR-mutant LAs in in vivo subcutaneous tumor models (Supplemental Figure 3, C–F). The gene discussed is EGFR; the disease is neoplasm.