Posttraumatic glutamate release and subsequent excitotoxicity is a major contributor to neuropathic pain following nerve injury. The loss of GABAergic tone caused by excitotoxicity further imbalances the inhibition and excitation of neural circuits, leading to further neuronal apoptosis. It has been established that inhibiting caspase can stop loss of GABA neurons post injury, and that stopping this loss prevents heat allodynia. Drosophila Twist knockdown show dampened hypersensitivity in response to nerve injury. Twist is heavily implicated in embryonic development, however its role in apoptosis is relatively unknown. We now aim to show the effects of twist knockdown in human GABAergic neurons grown from human induced pluripotent stem cells. We have successfully grown GABAergic neurons in a 28 day cell culture protocol derived from human induced pluripotent stem cells. We now plan to create twist knockdown cell lines using siRNA, and test the effects of glutamate stimulation on these cells compared with control cells; we hypothesise the twist knock down cells will show reduction in apoptosis.