It has been demonstrated that activation of β-catenin activity leads to tumor proliferation and reduced mouse survival in xenograft models, that EGFR tyrosine kinase inhibitor can activate β-catenin and Notch3 by inhibiting EGFR signal, and that knocking out Notch3 reduces β-catenin activity and resistance to targeted drugs (20, 46, 47). This evidence concerns the gene EGFR and neoplasm.