By suppressing TLR4 dimer assembly and lipid raft clustering, NAXE mitigates neuropathic pain in CIPN mice, linking membrane microdomain organization to inflammatory sensitization.361 Furthermore, in an amyloid beta precursor protein (APP)/presenilin 1 (PSEN1, also known as PS1) mouse model of Alzheimer’s disease, Loss of NAXE exacerbates microglial TLR4 clustering into inflammarafts, which drives: (1) bioenergetic collapse, (2) oxidative damage, (3) amyloid plaque accrual, and (4) neurodegeneration.362. The gene discussed is TLR4; the disease is early-onset autosomal dominant Alzheimer disease.