In the context of monogenic models, the failure of inhibitory synaptic drive is highlighted as a significant pathogenic stage, with genes like the serotonin receptor 5-HT2C playing a role in suppressing forebrain and brainstem networks, potentially leading to deadly induced audiogenic seizures 100, 101, 102 The SCN1A gene, commonly mutated in both epilepsy and SIDS infants, presents variants causing sodium channel dysfunctions that affect nerve and muscle action potential transmission, sometimes leading to death through seizures or without any epilepsy-like symptoms 103. This evidence concerns the gene SCN1A and epilepsy.