In the present study, we carry out our investigation to (a) examine the effects of Plk3 deletion in regulation of apoptosis in KrasG12D-induced PDAC development of genetically engineered mouse models; (b) better understand the function of Plk3 in activation of apoptosis in pancreatic cancer patient-derived cells (PDX); (c) elucidate the underlying mechanisms by which Plk3 is activated; and (d) most importantly, define the potential function of nardilysin (NRDC)-regulated post-translational modification. The gene discussed is NRDC; the disease is familial pancreatic carcinoma.