The results presented here make a strong case that abnormalities in microglia may not simply be a consequence of changes in other cell types involved in the pathophysiology of TSC, such as astrocytes and neurons, because we showed that the Tsc2+/− mutation restricted to microglia recreated the hippocampal memory deficits associated with animal models of TSC (7,9,36,45,46). The gene discussed is TSC2; the disease is tuberous sclerosis.