Although such an increase in LTB4 was attributed mainly to increased 5-LOX and LTA4H activities in neurons and astrocytes, the intense rise and co-localization of LTB4 with neutrophils (in our study) point to a significant contribution from neutrophils, probably through an increase in leukocyte infiltration into the brain from ischemia-induced inflammation, secretion of chemokines, and disruption of the blood-brain barrier [32]. The gene discussed is LTA4H; the disease is ischemia.