Indeed it has been shown that breast cancer cells with BRCA1/2 dysfunctions have a greater sensitivity to the PARP inhibitors because of the simultaneous ineffectiveness of both BER and HR mechanisms, respectively linked to the single (PARP inhibitors) and double (loss of function of BRCA1 and/or BRCA2) strand DNA damage, finally producing a chromosomal instability, cell cycle arrest and apoptosis [35, 71]. The gene discussed is PARP1; the disease is breast carcinoma.