Toverify whether the phosphorylation of Akt in HUVEC cells, treated or not with MβCD,was PI3K-dependent or -independent following infection with GBS90356 strain, thespecific PI3K inhibitor LY294002 was incubated prior to bacterial infection.Activation of the PI3K pathway occurred at 5 min post-infection and peak at 30 min.Both inhibitors reduced the PI3K phosphorylation (Fig.3B). This evidence concerns the gene AKT1 and bacterial infectious disease.