Bach1-deficient mice are more resistant to the oxidative stresses associated with trinitrobenzene sulfonic acid- (TNBS-) induced colitis [20], hyperoxic lung injury, nonalcoholic steatohepatitis [21], and cardiovascular disease [22], as well as bleomycin-induced pulmonary fibrosis [23], while declines in Bach1 expression or activity reduced measures of oxidative stress-induced apoptosis in pancreatic β-cells [24] and the damaging effects of ultraviolet radiation in keratinocytes [25]. This evidence concerns the gene BACH1 and colitis.