This image shows parvalbumin (yellow), β-catenin (red), and DAPI (blue) in an APC cKO mouse. In their article, Ryner et al. show that the maturation and survival of parvalbumin interneurons are disrupted in a model of early life epilepsy, known as infantile spasms. Inhibitory circuits are prominently shaped by development, so early life seizures may disrupt parvalbumin interneuron maturation. Conversely, inhibitory circuit dysfunction may contribute to seizure initiation, creating a potentially vicious cycle. By combining genetic models of infantile spasms, with anatomical and electrophysiological approaches, the authors shed new light on potential mechanisms of pathogenesis in a model of devastating early life epilepsy. For more information, see the article by Ryner et al. (pages 1422–1440). Cover image: Rachael Ryner and Mary Sommer.