Taking into account the elevated baseline levels of DNA damage and PARP activation in BRCA2-/- cells (Fig. 2A–C), we decided to measure PARP1 trapping after exposure to PARPi and in absence of any exogenous sources of DNA damage, aiming to reconstruct the molecular mechanisms that occur in HRR-deficient versus HRR-proficient cancer cells treated with PARPi monotherapy. The gene discussed is PARP1; the disease is cancer.