Collectively, our cross‐species validation of synthetic lethal interactions suggested that RAD51, FEN1, and PARL are likely essential in the presence of mutant KRAS‐driven signaling in colorectal cancer cells and, of these three, RAD51 is dysregulated in many cancers and has been identified as a potential target for drug discovery (Ward et al., 2015). Here, KRAS is linked to colorectal cancer.