Previous studies have shown that PHB2 directly binds to nuclear ERα, resulting in suppression of ERα transcriptional activity by competing with the co-activator SRC-1 to bind ERα [5] and by recruiting histone deacetylase 1 [HDAC1; ref. 6] and a co-repressor, NcoR [5, 6], in breast cancer cells, suggesting that PHB2 acts as a co-repressor of ERα. The gene discussed is HDAC1; the disease is breast carcinoma.