Recent studies have contributed significantly to our understanding of the molecular and cellular events that underlie the development of CNS radiation injury. Radiation-induced clonogenic cell death of "target cells" may not represent the sole mechanism of tissue injury. Apoptotic cell death and cell death arising from secondary injury may contribute to the development of long-term CNS injury. Specifically, cytokine cascades and stress responses associated with the damage deserve further investigations. These potentially reversible components of cell death present many targets for interventions using pharmacologic and biologic agents.