The mechanistic (or mammalian) target of rapamycin (mTOR) is a kinase that 
regulates key cellular functions linked to the promotion of cell growth and 
metabolism. This kinase, which is part of two protein complexes termed mTOR 
complex 1 (mTORC1) and 2 (mTORC2), has a fundamental role in coordinating 
anabolic and catabolic processes in response to growth factors and nutrients. Of 
the two mTOR complexes, mTORC1 is by far the best characterized. When active, 
mTORC1 triggers cell growth and proliferation by promoting protein synthesis, 
lipid biogenesis, and metabolism, and by reducing autophagy. The fact that 
mTORC1 deregulation is associated with several human diseases, such as type 2 
diabetes, cancer, obesity and neurodegeneration, highlights its importance in 
the maintenance of cellular homeostasis. Over the last years, several groups 
observed that mTORC1 inhibition, in addition to reducing protein synthesis, 
deeply affects gene transcription. Here, we review the connections between 
mTORC1 and gene transcription by focusing on its impact in regulating the 
activation of specific transcription factors including including STAT3, SREBPs, 
PPARγ, PPARα, HIF1α, YY1–PGC1α and TFEB. We also discuss the importance of these 
transcription factors in mediating the effects of mTORC1 on various cellular 
processes in physiological and pathological contexts.