In another study, using humanized HO-1 mice, where the human HO-1 gene, along with all its regulatory region, was inserted into mice with global HO-1 deficiency, it was revealed that the human HO-1 was functional, able to rescue the phenotype of HO-1 deficiency and conferred significant protection against rhabdomyolysis-induced AKI [112]. This evidence concerns the gene HMOX1 and rhabdomyolysis.