In conclusion, the results of this study demonstrated that 4E-BP1 activation regulated the amount of cell cycle re-entry provided by differentiated podocytes and the degree of podocyte apoptosis, opening the previously unthinkable possibility that in patients with glomerular disorders 4E-BP1 activity might be manipulated to ameliorate podocyte injury. The gene discussed is EIF4EBP1; the disease is glomerular disorder.