Recently, a growing body of evidence also showed that PARP‐2 inhibition served to resist tumor growth via induction of chromosome mis‐segregation, exacerbation of replication stress, and dysregulation of cancer epigenetics, which suggested that PARPs, especially PARP‐1 and PARP‐2, may be an attractive target for cancer therapy (Mégnin‐Chanet et al., 2010). The gene discussed is PARP2; the disease is cancer.