We then focused on the potential role of FOXM1 in AST, and found that FOXM1 overexpression had no major impact upon the protein levels of FOXA1 but did promote the upregulation of squamous markers (Fig. S10D–H) and the tumor volume increased ranging from 10% to 40% upon TKI treatments and maintained higher expression of squamous markers but lower expression of adenomatous markers (Fig. S10I–R). This evidence concerns the gene FOXA1 and neoplasm.