Consistent with the understanding that exposure to PARP inhibitors can enhance the burden of unrepaired DNA double-strand breaks (DSBs) by impeding PARP1 activity and PARP1 trapping onto damaged DNA [32], we demonstrated that olaparib-induced pharmacological inhibition of PARP1 synergistically enhanced the therapeutic effect of the FGFR1 inhibitor PD173074 and that olaparib alone or synergistically with PD173074 suppressed the oncogenic cancer stem cell-like phenotype of PDAC cells through the apoptosis-related impairment of DNA repair (Figure 4 and Figure 5). This evidence concerns the gene FGFR1 and cancer.