Proteomic analysis of CA1 regions following a hypoxic episode showed that the greatest fold change compared to control normoxia-treated slices concerned the downregulation of Adgrl1, responsible for functional synapse formation and maturation [23], in addition to the downregulation of Kctd4, responsible for potassium channel tetramerization, with the literature recently implicating the Kctd family of proteins in autism and schizophrenia via its role in the regulation of actin cytoskeleton dynamics [24]. The gene discussed is KCNA3; the disease is autism.