Moreover, in a kaolin-induced hydrocephalus model, toll-like receptor 4 (TLR4)-NF-κB signaling in the choroid plexus epithelium (CPE) stimulates CSF hypersecretion through the SPAK-NKCC1 cotransporter complex, thereby uncovering a novel kinase-regulated mechanism of CSF secretion (Heep et al., 2004; Xu et al., 2024) and the expression level of the TLR4–NF-κB signaling pathway was increased significantly in hydrocephalus after IVH. The gene discussed is NFKB1; the disease is Hydrocephalus.