However, inhibition of the MCP-1/CCR2 axis with drugs could downregulate CCR2, but it was not sufficient to prevent acute kidney injury from progressing to CKD or to improve renal fibrosis in mice with U-IRI.[69] Similarly, Salah et al performed MCP-1 genetic knockout in mice with congenital polycystic kidneys to test whether deletion of MCP-1 reduced renal macrophage infiltration and slowed disease progression. The gene discussed is CCL2; the disease is polycystic kidney disease.