Germline pathogenic variants in individuals with TSC were predominant in TSC2, as previously established.41,47 In those with FCDII/HME, we identified somatic pathogenic variants in genes spanning the full PI3K-AKT-mTOR and GATOR1 complex pathways, without a clear preponderance of one gene, highlighting that the causative gene does not necessarily predict the type of epilepsy.48 The range of mTOR pathway genes in our cohort may reflect the variable size of malformations in these individuals. The gene discussed is TSC2; the disease is epilepsy.