Several studies have suggested that Tsc1 mutation in the patients with human tuberous sclerosis complex have caused immune activation, which might further contribute to the development of the disease.30, 31, 32, 33 The spontaneous T-cell activation and lymphoproliferative disease in mice lacking Tsc1 in DCs implies that disruption of Tsc1-dependent DC function may be a mechanism underlying the immune activation phenotype in human tuberous sclerosis complex patients. The gene discussed is TSC1; the disease is tuberous sclerosis.