Recent data from Ellisen and colleagues suggest that a primary Ddit4 mechanism of action is to competitively bind inhibitory 14-3-3 proteins that otherwise bind to the Tsc2 protein, part of the tuberous sclerosis complex that inhibits Akt/Frap1 signaling when Tsc2 is unbound [32]. This evidence concerns the gene DDIT4 and tuberous sclerosis.