PARP depletion in acinar tumours in vivo was demonstrated to decrease proliferation, increase cell death and reduce acinar-to-ductal metaplasia (ADM) by driving clonal expansion of the prognostically favourable acinar malignant cells, suggesting PARPi as a promising therapeutic in early pancreatic cancer oncogenesis [77]. The gene discussed is PARP1; the disease is pancreatic neoplasm.