To investigate this hypothesis, we used constitutive and inducible KO mouse lines and analyzed the impact of deletion of the Usp15 gene on epilepsy-dependent histological changes and downstream modulation of IFN-α/β, TGF-β, and NRF2 pathways acutely after status epilepticus and determined whether this has disease-modifying effects in chronic epilepsy. Here, USP15 is linked to status epilepticus.