Hence, our series alsosupports that, in patients with a neurodevelopmental phenotype, HMEG or MEG withoutapparent brain malformation might be more suggestive of pathogenic variants inMTOR rather than in PIK3CA or AKT3, as previouslyoutlined.22–25 Interestingly, the structure and function ofhomogeneously enlarged brains with postzygotic MTOR pathogenic variants may be less altered than of those withHMEG. The gene discussed is PIK3CA; the disease is cerebral malformation.