Supportive of compensatory roles, co-deletion of PARP1 and PARP2 results in embryonic lethality (Menissier De Murcia, 2003), however, PARP1−/− mice exhibit increased spontaneous tumor incidence suggesting PARP2 cannot fully compensate for PARP1 loss (Shibata et al., 2009). This evidence concerns the gene PARP2 and neoplasm.