Treatment with LCN-2 mAbs significantly attenuates LCN-2 mRNA and protein within a clinically relevant time window; however, targeting LCN-2 to inhibit post-stroke neuroinflammation may be more beneficial than inhibiting individual cytokines and chemokines, as LCN-2 may be responsible for the inflammatory cascade important upstream regulators of these mediators. Here, LCN2 is linked to stroke disorder.