The initial discovery of the SL interaction between BRCA1/2 and PARP1 in breast cancer (BRCA) and ovarian cancer (OV) is the pivotal example of the bench to bedside translational potential of SL and has paved the way for the use of PARP inhibitors (PARPi) in other tumor types characterized by homologous recombination repair (HRR) gene mutations (1, 2). This evidence concerns the gene PARP1 and breast carcinoma.