In our study, since interferon expression can be induced in endothelial cells[62], and thus floxed target genes can be inactivated homozygously in renal endothelial cells in adults by the Mx-Cre/loxP recombination system [63] without damaging vascular development, these results give further evidence of the crucial role of HIF-2α in the protection against endothelial dysfunction in acute ischemic renal injury. The gene discussed is MX1; the disease is endothelial dysfunction.