The inactivation of GSK3β by phosphorylation, carried out mainly by Akt, may result in the activation of transcription factors such as AP-1 (Jun family), cAMP-response element binding protein (CREB), signal-transducer and activator of transcription 1-3 (STAT1-3), β-catenin, and nuclear factor-kappaB (NF-κB) in response to bacterial infections [2,3] (Figure 1). This evidence concerns the gene AKT1 and bacterial infectious disease.