Taken together, the significant glomerular upregulation of IL-33 in patients with DKD, the substantial kidney-protective effect of suppression of IL-33/ST2 signaling in the db/db unx mouse model of DKD, and the molecular function of IL-33 as a significant glomerular amplifier of inflammation underscored the potential clinical benefit of IL-33 blockade by tozorakimab in patients with DKD. Here, IL33 is linked to diabetic kidney disease.