MYC gene expression is estrogen-responsive and expression of MYC and CCND1 contribute to the proliferative response stimulated by estrogen treatment (Dubnik et al, 1987; Dubnik et al, 1988; Dubnik and Shu, 1992; Prall et al, 1998). Estrogen-responsive MYC expression appears to depend at least in part on a distal enhancer element 67 kb from the transcriptional start site that contains a half ERE and an AP-1 site (Denardo et al, 2005; Carroll et al, 2006; Wang et al, 2011). Upon estrogen stimulation, these sites are occupied by ESR1 and a JUND:FOSB heterodimer, respectively (Wang et al, 2011). Estrogen-responsive MYC expression also depends on the cohesin complex, as depletion of the RAD21 cohesin subunit abrogates expression (Stedman et al, 2008; Schmidt et al, 2010; McEwan et al, 2011; Antony et al, 2015). Genome-wide studies have shown that RAD21 and ESR1 binding sites overlap in a fraction of estrogen-responsive genes, including MYC (Schmidt et al, 2010). Cohesin may contribute to target gene expression by promoting chromatin looping structures between distal enhancers and the target gene promoters or through other mechanisms that remain to be elucidated (Li et al, 2012; Antony et al, 2015; reviewed Rhodes et al, 2011; Losada, 2014). Overexpression of histone isoform HIST1H2AC in breast cancer has been shown to contribute to MYC gene expression by promoting the formation of activating chromatin loops and facilitating the recruitment of ESR1, EP300 and RNA polymerase II (Su et al, 2014).