In a mouse model of posthemorrhagic hydrocephalus, Toll-like receptor 4–nuclear factor kB (NF-kB) signaling has been described as an important pathway in mediating hydrocephalus development by causing further damage to the ependymal cells or CSF hypersecretion from the choroid plexus epithelium (Karimy et al., 2017; Simard et al., 2011). This evidence concerns the gene TLR4 and Hydrocephalus.