Although major advancements in the generation of RNAi and CRISPR/Cas9 libraries have undoubtedly advanced our ability to uncover potential SSL relationships at the genome scale, the most successful implementation of an SSL strategy to date in cancer treatment, the targeting of BRCA‐deficient cells with PARP1 inhibitors, was derived from hypothesis‐driven research rooted in a fundamental understanding of the specific molecular pathways concerned and relevant interplay between them, rather than broad screening approaches [138, 139]. The gene discussed is PARP1; the disease is cancer.