The tuberous sclerosis gene 2 product tuberin is an important regulator of the 
mammalian target of rapamycin (mTOR). In addition, tuberin is known to bind to 
the cyclin-dependent kinase (CDK) inhibitor p27(Kip1) (p27) and to regulate its 
stability and localization via mTOR-independent mechanisms. Recently, evidence 
has been provided that tuberin also affects p27 localization via regulating 
mTOR's potential to activate the serum- and glucocorticoid-inducible kinase 
(SGK1) to phosphorylate p27. Taken together, these findings strengthen the 
argument that besides mTOR-inhibitors, such as rapamycin analogues, p27 and CDKs 
could also be considered targets for hamartoma therapeutics in tuberous 
sclerosis.