HDACs are important in fibrosis in organs other than the CD intestine.23–25 H3K27ac levels have been used as a proxy for HDAC activity in a mouse model of colitis, and IBD patients with active disease.13 Moreover, histone acetylome studies using H3K27ac have identified chromatin-mediated gene expression changes during fibrosis in other organs.26 Here, we show that SCD tissue exhibited a reduced percentage of H3K27ac+ cells in the mucosa and muscularis propria, suggesting hypoacetylation is present in all SCD intestinal layers. This evidence concerns the gene HDAC9 and colitis.