In addition, gliotoxin can ameliorate trinitrobenzene sulfonic acid (TNBS)-induced mouse colitis via the suppression of the expression levels of TNF-, IL-1, and intercellular adhesion molecule-1 (ICAM-1) proteins as well as the upregulation of heme oxygenase-1, thus indicating the potential application of gliotoxins in the clinical treatment of Crohn’s disease [50] via the induction of hemooxygenase-1, which can oxidize low-density lipoproteins with the potential to form chemo-attractants, thus alleviating the inflammation [51]. The gene discussed is TNF; the disease is colitis.