Competing with the cofactor NAD+ to interact with the enzyme’s binding site [7], PARP inhibitors both inhibit catalytical poly-ADP-ribosylation (PARylation) of target proteins but at the same time can hamper the function of the replication fork by trapping the enzyme on the DNA [8] in a not yet fully understood process, ultimately leading to enhanced susceptibility of the tumor for DNA-damaging agents [9–11]. Here, PARP1 is linked to neoplasm.