In a mouse model of temporal lobe epilepsy, activation of TRPV4 increased Toll-like receptor 4 (TLR4) expression, which led to the phosphorylation of IκK and IκBα; as a result, NF-κB activation and nuclear translocation occurred, with a resulting increase in the levels of pro-inflammatory cytokines.197 Thus, blocking TRPV4 downregulates high mobility group box 1 (HMGB1)/TLR4/IκK/κBα/NF-κB signaling, which produces an anti-inflammatory response and neuroprotective capacity.197. This evidence concerns the gene NFKB1 and temporal lobe epilepsy.