Induction of apoptosis, as evidenced by the proteolytic cleavage of PARP1 (inactivation) and Caspase-3 (activation) in the BxPC-3 cells, and, to a lesser extent, in the AsPC-1 (magnified at 48 h) and PANC-1 (hardly detectable) cell lines, along with the severe reduction in Survivin protein contents in response to TH301 exposure in all three (PDAC) cell lines examined herein, supports the (pro-)apoptotic capacity of TH301 in human pancreatic cancer cells of diverse mutational background. The gene discussed is PARP1; the disease is pancreatic neoplasm.