Intriguingly, the functional analysis of a cancer-associated STAG2 S202L mutation, which is proficient for sister chromatid cohesion, but not transcriptional repression at DNA breaks suggests that one putative mechanism by which STAG2 functions as a tumor suppressor is through its role in promoting accurate repair at DSBs that occur in the vicinity of actively transcribed genes [62]. The gene discussed is STAG2; the disease is neoplasm.