Using a mouse model of tuberous sclerosis complex, a neurodevelopmental disorder involving epilepsy, in which the Tsc1 gene was conditionally deleted in forebrain, BMAL1 activity was shown to be upregulated in an mTOR-dependent manner and reduction of BMAL1 to control levels was able to rescue the mutant phenotype (149). Here, BMAL1 is linked to tuberous sclerosis.