It is known that the number, proliferation, and function of EPCs decline in patients with aging, cardiovascular risk factors, or diabetes.23–26 Recently, we reported that autologous granulocyte-colony stimulating factor (G-CSF)-mobilized PB-CD34+ cell transplantation for patients with decompensated LC had therapeutic potential, but the colony-forming ability of patients with decompensated LC had been reduced.5Ex vivo expansion of autologous cells is indispensable for cell transplantation therapy of patients with chronic disease including LC. This evidence concerns the gene CSF3 and laryngotracheoesophageal cleft.