The main results of the present study are as follows: (1) significant increases in HDAC2 and HDAC3 (Figure 3) and (2) the down-regulation of KCa3.1 by the pharmacological inhibition of HDAC2 or HDAC3 in the inflammatory CD4+ cells of IBD model mice (Figure 5). The gene discussed is KCNN4; the disease is inflammatory bowel disease.