Abstract
The non-canonical functions of the transcription factor STAT3 have been poorly studied in comparison to its canonical mechanisms of gene expression activation. Here, Köhler etal. put the spotlight on a novel unconventional repressing mechanism of STAT3 over the REDD1 gene, named DDIT4. These findings are crucial to expand the knowledge of the stress-induced short-lived REDD1 protein that inactivates mTOR and the consequences of this fine-tuned regulation in the context of pathological conditions such as cancer or neurodegenerative diseases.
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