In mice model of IRI-induced AKI, IL-33 was passively released by dying endothelial cells and bound to ST2 as a ligand, which induced the conversion of proinflammatory M1 macrophages into anti-inflammatory M2 macrophages, reducing the release of proinflammatory factors, whereas IL-33 promotes the expansion of type II innate lymphoid cells (ILC2s) and Tregs, improving the immune microenvironment and reducing renal inflammation (88, 89). The gene discussed is IL33; the disease is acute kidney injury.