S the site of highestJNK expression, and all single-JNK knockout mice have CNS defects to a variable degree (reviewed in reference 2). Since normal JNK activity is implicated in neuronal development and regeneration but overactivation of JNK can induce apoptosis of neurons, inhibitors of JNKs or their upstream regulators have been proposed as desirable neuroprotective agents (398?00). These observ