Data generated in this study provide mechanistic insight into why breast cancer cells may be selectively sensitive to HDAC inhibitors compared to normal breast epithelium; down-regulation of ING1 would already reduce the ability of cancer cells to accurately target the Sin3A complex and so treatment with HDAC inhibitors such as SAHA that selectively target ING2 and/or ING1 would be expected to have greater effects upon the epigenomes of cancerous versus normal epithelial cells. This evidence concerns the gene ING1 and breast carcinoma.