Interestingly, NF-κBp65 deficiency in gastric myeloid cells inhibited FasL expression, followed by Fas downregulation, revealing that IL-6-driven FasL in myeloid cells contributed to the epithelial apoptosis via Fas in PHG, which is consistent with the observation that immune cells could facilitate the integration of the pathophysiological mechanisms involved in the different complications of portal hypertension, such as PHG. The gene discussed is IL6; the disease is portal hypertension.