Most of the therapeutic strategies using PARP inhibitors rely on their blockade of DDR and the creation of synthetic lethality in combination with genetic defects in homologous recombination-mediated repair (Farmer et al., 2005; Lord and Ashworth, 2017; McCabe et al., 2006), which are the basis for the treatment of patients with BRCA1- and BRCA2-associated cancers (Mateo et al., 2019). This evidence concerns the gene PARP1 and cancer.