Neuroinflammation plays a critical role in various neurological conditions, particularly in the context of neurosurgery. Recent studies have highlighted the choroid plexus (ChP) as a pivotal player in linking innate immunity to cerebrospinal fluid (CSF) dysregulation in hydrocephalus. An integrated multi-omic investigation revealed that lipopolysaccharide and blood breakdown products trigger TLR4-dependent immune responses at the ChP-CSF interface, suggesting a potential therapeutic target for post-infectious and post-hemorrhagic hydrocephalus (ref: Robert doi.org/10.1016/j.cell.2023.01.017/). Additionally, the interactions between innate immune cells and astrocytes have been shown to facilitate neuroinflammation and brain metastasis, particularly through the action of granulocyte-derived lipocalin-2 (LCN2), which activates astrocytes and recruits myeloid cells to the brain, indicating a complex interplay that could be exploited for therapeutic interventions (ref: Adler doi.org/10.1038/s43018-023-00519-w/). Furthermore, the identification of master kinases such as PKCĪ“ and DNA-PK in glioblastoma subtypes through integrative multi-omics networks underscores the importance of targeting specific pathways in glioblastoma therapy (ref: Migliozzi doi.org/10.1038/s43018-022-00510-x/). These findings collectively emphasize the need for a deeper understanding of neuroinflammatory mechanisms to develop effective treatments for neurological disorders and brain tumors.