Our previous findings indicated that the up-regulation of class I HDACs (HDAC2 and HDAC3) contributed to the increased expression and activity of KCa3.1 in the CD4+ cells of the IBD model mice; however, class I HDAC inhibitor-induced decreases in the expression levels of K2P5.1 transcripts were not found [13]. Here, KCNN4 is linked to inflammatory bowel disease.