On the other hand, Akt inhibits GSK3β by phosphorylation at residue Serine9 [72] and Akt phosphorylation and activation in a phosphatidylinositol 3-kinase (PI3K)- and lipid raft formation-dependent manner as a response to viral infections with cytoplasmic RNA viruses has been demonstrated (e.g., the DENV and the JEV) [73]. This evidence concerns the gene AKT1 and viral infectious disease.