In cancer cells, however, 4E-BP1 is frequently hyperphosphorylated by its upstream oncogenic signals such as PI3K/AKT and RAS/RAF/MEK/ERK pathways, which causes 4E-BP1 disassociation from eIF4E and thus inactivates 4E-BP1 function and increases the level of free eIF4E. The gene discussed is AKT1; the disease is cancer.