Given that several lines of evidence strongly suggest that cancer cells with HR deficiency (e.g. through BRCA1/2 inactivation) show a significant hypersensitivity to PARP inhibition [17], [19], [20], [21], [24], [26], and given that hMOB2 deficiency impairs HR in cancer cells (see Fig. 1, Fig. 2, Fig. 3), we next sought to determine whether hMOB2 loss has a synthetic lethal interaction with PARP inhibition. The gene discussed is BRCA1; the disease is cancer.