We hypothesised that migraine would be associated with increases in CD8+ T cells, classical monocytes, PLAs, changes in T-cell effector function, and upregulation of the p38 MAPK-MK2-NFκB axis as we have observed in other chronic pain conditions.19,29,34 We also hypothesised phase-dependent differences in short-lived neutrophils and platelets, stable T-cell signatures associated with activation and memory across the migraine cycle, and increased proinflammatory proteins, QUIN, and MMP-9. The gene discussed is NFKB1; the disease is migraine disorder.