TSC2 and epilepsy: TSC-associated missense variants were more common in TSC2 than in TSC1, and particularly occurred in the GAP domain, indicating its pivotal role in the function of hamartin-tuberin complex.21 Several animal models, including conventional and conditional Tsc2 knockout mice, showed epilepsy, brain anomalies, and tumors in kidney, spleen, and uterus.22,23 Mice heterozygous for loss of Tsc2 exhibited more severe TSC-associated features and occurred earlier than those with heterozygous loss of Tsc1. 5,24