In murine models of sepsis, the presence of LPS at the systemic level induces the upregulation of Toll-like receptors (TLR1, TLR2, TLR3, TLR4), CD14, cyclooxygenase-2 (COX-2), nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, and alpha (IκBα) in choroid plexus cells, which can lead to the decreased expression of occludin in the CSBFB [83,84,85,86,87,88,89]. The gene discussed is NFKBIA; the disease is Sepsis.