It is probable that the CCK+/CB1R+ interneuron axon targeting and synapse phenotypes in the mouse models described in the present study contribute to their seizure susceptibility and open the possibility that defective inhibitory synaptic signaling mechanisms may underlie seizures in dystroglycanopathy patients. The gene discussed is CCK; the disease is neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan.