AKT1 and cancer: More recently, we found that SIRT7 interacted with FKBP51, and deacetylated FKBP51 at lysines 28 and 155 residues (K28 and K155), thereby resulting in enhanced interactions among FKBP51, AKT, and PHLPP, and culminated in AKT dephosphorylation and subsequent sensitization of cancer cells against gemcitabine12.