Both forms are caused by mutations in the tuberous sclerosis genes TSC1 and TSC2, resulting in the loss of function of their protein products hamartin and tuberin, respectively; this leads to inappropriate signaling through the mammalian target of rapamycin (mTOR) pathway, with its constitutive activation, promoting cell growth and proliferation [2,4]. This evidence concerns the gene TSC2 and tuberous sclerosis.