In summary, CRISPR/Cas9 was designed and optimized to disrupt PARP1, the synthetic lethal pair of BRCA1. While the 2D in vitro results showed that CRISPR/Cas9‐mediated PARP1m sensitized the TNBC cells with BRCA1m to chemotherapeutic drugs, there was a dichotomy between the 2D and 3D tumor‐on‐a‐chip results, mirroring inconsistencies found in recent clinical trials. This evidence concerns the gene BRCA1 and neoplasm.