AKT1S1 and infection: The regulation of NF-κB activity by various stimuli such as cytokines or infection requires the degradation of IκB α, which unmasks and releases p65 from the cytoplasm into the nucleus.15, 26 However, our results showed that altered expression of PRAS40 did not impact phosphorylation of IκBα (Supplementary Figure S1), which may indicate that PRAS40 promotes the transcriptional activity of NF-κB by binding to P65 in the nucleus or through another non-canonical mechanism.