Posttranslational modifications of ERα, such as phosphorylation and poly-/mono-ubiquitination, appear to be central for the modulation of its stability, transport, and localization, and some may compete by the same site to modulate ERα stability and activity; for example, K303 is acetylated, mono- and poly-ubiquitinated in breast cancer cells (66, 73, 76, 113, 149), and some mutations at K303 exist in premalignant breast lesions (150, 151). This evidence concerns the gene ESR1 and breast carcinoma.