To the editor:I read with great interest the recent article by Liu et al.1 The article provided highly interesting data on the mitigating effect of flurbiprofen on ischemia related injury.Interestingly,besides affording neuroprotection by activation of cerebral peroxisome proliferator activated receptor gamma,flurbiprofen also affords cerebral protection after ischemia/reperfusion injury by modulating the Akt/GSK-3β pathway.2 It also up regulates Bcl-2 expression.At the same time it doewnregulates the expression of Bax.3 As a result,there is a marked decrease in neurological deficit scores.P-Akt levels are also accentuated markedly.As a result intra cerebral apoptosis is markedly attenuated resulting in a decrease in infarct volume.Flurbiprofen is also an acid sensing ion channel protein (ASICla)inhibitor.4 As a result,it attenuates ischemic associated increases in malondialdehyde (MDA) levels as well has a mitigatory effect on calpain mediated increase in spectrin breakdown products (SBDPs).The neuro-protection afforded by flurbiprofen is further augmented by using agents such as ifenprodil in conjunction with flurbiprofen.5 Ifenprodil is an NR2b selective N-methyl-D-aspartate receptor (NMDAR) antagonist and further reduces the infarct size.The advantage of flurbiprofen is that the therapeutic time window can be as long as 24 hours.