Indeed, in addition to a physical binding and functional inactivation of p53, HB×Ag promotes fibrogenesis by stimulating fibronectin expression, inhibits apoptosis mediated by Fas and tumor necrosis factor-alpha (TNF-α) and its expression correlates with the development and progression of CLD [102,103]. The gene discussed is TNF; the disease is congenital secretory chloride diarrhea 1.