The model presented here differs in that only Tsc2 was removed and has the additional advantages of low mortality, no seizure activity allowing for distinguishing seizure-dependent and seizure-independent changes, and focal hamartomas which mimics that seen in patients and therefore affords the tracking of cells and delineation of cell autonomous and intercellular effects of loss of Tsc2. Nevertheless, these results argue that rodents can generate hamartoma-like lesions and that deletion of TSC genes in neonatal V-SVZ NSCs can sufficiently model TSC. The gene discussed is TSC1; the disease is tuberous sclerosis.