Two working models have been proposed for the mechanism whereby REDD1 acts to suppress mTORC1. In both models, the suppressive effect of REDD1 on mTORC1 is mediated by a reduction in the proportion of GTP bound to Rheb. In the first model, REDD1 binds 14-3-3 protein to prevent TSC2 sequestration in an inactive complex. In the second, REDD1 promotes dephosphorylation of Akt at Thr308 by PP2A. Akt-dependent phosphorylation of TSC2 suppresses the GAP activity of TSC2 toward Rheb. In addition, REDD1-dependent dephosphorylation of Akt also influences other important targets downstream of Akt, including FOXO transcription factors and GSK3.