In a FA-induced AKI mouse model, genetic deletion of IL-18 markedly reduces the expression levels of key regulators of epithelial–mesenchymal transition (EMT), including TGF-β1 and vimentin, along with a marked decrease in collagen type I (COL-1), a hallmark marker of renal fibrosis, further highlighting the profibrotic role of IL-18 in the AKI-to-CKD transition [191]. The gene discussed is IL18; the disease is renal fibrosis.