Thus, based on the findings of Yuan et al., we suggest that FGFR1- and PARP-rich pancreatic cancer cells maintain their insensitivity to single-agent FGFRs and evade cell death by suppressing TRAIL-associated apoptotic DNA fragmentation by caspase-activated DNase/DNA fragmentation factor 40 endonuclease, thus suggesting a critical role of DNA damage/repair balance in pancreatic cancer therapy response [26,27]. The gene discussed is PARP1; the disease is familial pancreatic carcinoma.