To dissect potential underlying mechanisms, Dev et al. performed whole-genome CRISPR-Cas9 synthetic-viability/resistance screening in BRCA1-deficient breast cancer cells treated with PARP inhibitors and identified that the resistance of breast cancer cells to PARP inhibitor was, at least in part, due to loss of C20orf196 and FAM35A (166). This evidence concerns the gene SHLD2 and breast carcinoma.