The major causes of mortality in patients with TSC are seizures and renal complications.[2] TSC is believed to have a high spontaneous mutation rate, as suggested by the large number (approximately two-thirds of all cases) of aperiodic cases without a family history.[3]TSC1 and TSC2, which act as tumor growth suppressors and encode the proteins hamartin and tuberin, have been found to be responsible for mTOR overactivation, which may be the underlying mechanism of pathogenesis.[4]. Here, TSC2 is linked to neoplasm.