In some cases, it manifests as symptomatic epilepsy associated with cortical developmental malformations, with the interaction between CUL4B and WDR62—linked to various brain malformations—potentially playing a role.522 However, in other cases, epilepsy does not appear to be related to cortical malformations but may instead arise directly from the gene’s impact on neuronal excitability.522 Functional studies examining the effects of pathogenic variants identified in patients with seizures are essential to validate this hypothesis. Here, WDR62 is linked to epilepsy.