In support of this idea, treating multiple gefitinib-resistant lung cancer cells (including HCC4006GR, H2279 and HCC827-ZEB1) with BMS-708163 or DAPT (another γ-secretase inhibitor) also reversed their resistance phenotype to various extents (Fig. 7b–d), demonstrating that NOTCH activation exerts a universal biologic function in EGFR inhibitor resistance in lung cancer cells, and that NOTCH inhibitors may have a therapeutic value in treating EGFR inhibitor-resistant lung tumours. The gene discussed is EGFR; the disease is lung cancer.