The synergistic effect of AZ1 and targeted therapy does not only stem from impairment of tumour cell proliferation but also leads to onset of cell death, as seen by Ki‐67 expression and PI incorporation experiments of BEAS‐2BONC cells cultivated for 72 h in the presence of the single compounds or combinations thereof at synergistic concentrations (AZ1: 7.5 μm, gefitinib: 7.5 μm; buparlisib: 0.5 μm; and vemurafenib: 7.5 μm; Fig. 7G,H). The gene discussed is MKI67; the disease is neoplasm.