In our previous study, we found that an upregulation of DCLK1 could maintain tumor cell stemness through activation of the Wnt/β-catenin pathway and, subsequently, mediate EGFR-TKI-acquired resistance, while the application of Wnt/β-catenin pathway inhibitors only partially restored the reduced TKI sensitivity due to DCLK1 high expression, implying additional mechanism involved in TKI-acquired resistance [27]. This evidence concerns the gene EGFR and neoplasm.