Having shown that the pharmacological inhibition of PARP1 expression synergistically enhances the therapeutic effects of the FGFR1 inhibitor PD173074 through a caspase-dependent apoptotic mechanism, against the background that the cleavage/activation of caspases induces DNA fragmentation, cytoskeletal and nucleosomal degradation, protein cross-linking, the formation of apoptotic bodies, and phagocytosis, with subsequent cell death [17,18], we further sought to understand the effect of this synergism on the cancer stem cell-like phenotype of PDAC cells. Here, PARP1 is linked to cancer.