When compared with either condition (Fig. 4D and Fig. S10J), combined FOXM1 overexpression and FOXA1 knockout resulted in a notable TKI-resistant phenotype with 30%–80% tumor volume increase and maintained higher expression of squamous markers but lower expression of adenomatous markers upon drug treatments (Fig. 5D–G and Fig. S11A–F), reminiscent of the DR tumors (Fig. S1B). The gene discussed is FOXA1; the disease is neoplasm.