DCAMKL2 (also known as doublecortin-like kinase 2 or DCLK2) is a close homologue of doublecortin or DCX which is associated with intractable epilepsy in humans, due to a severe disorganization of the neocortex and hippocampus known as classical lissencephaly. DCX; DCLK2-null mice display frequent spontaneous seizures that originate in the hippocampus, with most animals dying in the first few months of life. DCX and DCLK2 are co-expressed in developing hippocampus, and, in their absence, there is dosage-dependent disrupted hippocampal lamination associated with a cell-autonomous simplification of pyramidal dendritic arborizations leading to reduced inhibitory synaptic tone (1).