Similar compensatory mechanisms have been identified in other models such as the downregulation of multiple potassium channels in a sodium channel (Scn2a) LOF mouse model of epilepsy, resulting in neuronal hyperexcitability (Zhang et al., 2021), or the upregulation of Na+ currents in response to increased potassium channel activity in a developing Xenopus neural circuit, resulting in restored intrinsic excitability and network stability (Pratt and Aizenman, 2007). The gene discussed is SCN2A; the disease is epilepsy.