In NPH-mouse models and urine-derived kidney epithelial cells (UREC) from NPH patients, we showed increased expression of inflammatory chemokines, including CCL2, CX3CL1, CXCL1, and CXCL10, which is associated with infiltration of macrophages, neutrophils, and T cells into the kidney, supporting that inflammation is a central feature of renal ciliopathies. The gene discussed is CXCL1; the disease is normal pressure hydrocephalus.