This contrasts with an earlier study showing that long-term overexpression of Kim1 in epithelial lineages increases expression of inflammatory markers and increases renal fibrosis (30), and it suggests that while short-term upregulation of Kim1 in PTEC DN RAR mice protects against AKI, long-term Kim1 overexpression results in proinflammatory kidney injury and fibrosis. This evidence concerns the gene HAVCR1 and renal fibrosis.