Tuberous sclerosis complex (TSC) is a relatively rare autosomal dominant 
disorder characterized by widespread benign tumor formation in a variety of 
organs. Mutations in either TSC1 or TSC2 tumor suppressor gene are responsible 
for TSC. The gene products of TSC1 and TSC2, also known as hamartin and tuberin, 
respectively, form a physical and functional complex and inhibit the mammalian 
target of rapamycin complex 1 (mTORC1) signaling. The mTORC1 pathway is an 
evolutionarily conserved growth promoting pathway. mTORC1 plays an essential 
role in a wide array of cellular processes including translation, transcription, 
trafficking and autophagy. In this review, we will discuss recent progresses in 
the TSC-mTOR field and their physiological functions and alterations of this 
pathway in pathophysiology.