Downregulation was due to a lack of phosphorylated AKT(Ser473) and NF-κB/p65(Ser536), which rapidly takes place after adhesion to E-selectin by AML blasts in vitro, thereby suggesting that AKT phosphorylation may be a potential mechanism to promote chemoresistance [35]. Here, AKT1 is linked to acute myeloid leukemia.