Conditional deletion of HDAC2 alone was shown to protect against DSS [62], however, and in contrast to the benefits of HDAC inhibition, deletion of both HDAC1 and 2 in mice seems to enhance sensitivity to induced colitis and disrupts epithelial barrier function [62–64], indicating that at least some activity is necessary to rip the protective benefits. This evidence concerns the gene HDAC1 and colitis.