Gene ontology analysis of these overlapped genes revealed that SIN3A/3B/SAP30-corepressed genes were involved in development of multiple organs, which was consistent with previous findings (13); whereas angiogenesis- and cell migration–related pathways were highly enriched among SIN3A/3B/SAP30-coactivated genes (Figure 7C), which supported SAP30/SIN3A/3B-mediated tumor phenotypes in breast cancer mouse models (Figures 2–4). The gene discussed is SAP30; the disease is breast cancer.