Moreover, deletion of the Nrp2 ligand, semaphorin 3 F (Sema3F), in GABAergic neurons resulted in increased seizure susceptibility [24] and development of autism-like behaviors [25], suggesting that mice with deficient Nrp2 signaling could serve as a model to assess inhibitory circuit dysregulation associated with the propensity for autism/seizure phenotypes. The gene discussed is SEMA3F; the disease is autism.