Potential pitfalls related to the timing of treatment have been revealed after delivery of neutralizing antibodies against the axonal growth inhibitor NogoA, which, when administered prior to stroke, augmented ischemic injury in a mouse model of transient middle cerebral artery occlusion as a consequence of the early promotion of energy-requiring neuronal growth that resulted in the activation of cell death pathways. This evidence concerns the gene RTN4 and stroke disorder.