Evidence for the involvement of Nrf2/HO-1 pathway in the course of UC was first published in 2006, when it was reported that DSS-induced colitis was associated with increased expression of Nrf2 regulatory enzymes and that the increased susceptibility of Nrf2-deficient mice to DSS-induced colitis may be due to decreased expression of HO-1 as well as increased expression of proinflammatory mediators [24]. This evidence concerns the gene HMOX1 and colitis.