RAS/ERK signaling is known to regulate JUN at the transcriptional and post-translational (phosphorylation) level and can modify lysine acetylation in JUN DNA binding regions.47 Recent studies have demonstrated that AR is expressed in 77% of breast cancers (88% ER+, 59% HER2+, 32% TNBC)48 and is involved in endocrine resistance in ER+ breast cancers.49,50 Although there are studies demonstrating interaction of C/EBPα at ER transcriptional binding sites, the consequence of C/EBPα activity in breast cancer is unclear. The gene discussed is JUN; the disease is breast carcinoma.