Mutations in tuberous sclerosis complex 1 (TSC1) and tuberous sclerosis complex 2 (TSC2) that lead to hyperactivation of the target of rapamycin (TOR) pathway are causative of tuberous sclerosis, a hamartoma syndrome associated with a predisposition to malignancy [3], and heterozygous Tsc1 or Tsc2 mutant mice develop renal and extrarenal tumors such as hepatic hemangiomas [4]. This evidence concerns the gene TSC1 and Hepatic hemangioma.