We do know that HO-1 plays a cytoprotective role in a rodent model of RM-AKI [2, 3], and the deletion of the Bach1 gene in mice confers protection against acute oxidative tissue injuries, including those to the cardiovascular system, respiratory tract, digestive tract, liver, and skin, which are mediated through the overexpression of HO-1 [28]. This evidence concerns the gene BACH1 and acute kidney injury.