KCNA2 and fragile X syndrome: Knowing that Kv1.2 are particularly abundant in interneurons, under-expression of these channels is likely a common feature of presynaptic dysregulation of inhibition, and may contribute to a variety of pathological phenotypes associated with FXS, autism, and seizure which are exhibited by Kv1.2 mutant mice or polymorphisms observed in humans [30, 57].