The concept of applying PARPi to treat HR‐deficient cancers has largely been based on the fact that PARP inhibition impairs base excision repair (BER) and single‐strand repair (SSR), therefore leading to the accumulation of DNA double‐strand breaks (DSBs), which cannot be fixed by defective HR repair (Bryant et al, 2005; Farmer et al, 2005). The gene discussed is PARP1; the disease is cancer.