Together with the analysis of the cancer-associated S202L mutation of SA2, which is proficient for sister chromatid cohesion, but not transcriptional repression at DNA breaks (Figure 4), these data raise the possibility that one mechanism by which SA2 functions as a tumor suppressor gene is through its role in promoting accurate repair at DNA DSBs that occur in the vicinity of actively transcribed genes. The gene discussed is STAG2; the disease is neoplasm.