,37 Hepatocytes are known to be a major source of VEGF within the liver,38,39,40 and we confirmed that a hepatocyte-endothelial axis could be important for PLVAP regulation in CLD, showing that supernatants from hepatocyte cell line, HepG2, also upregulated PLVAP in LSEC (Figures S4F and S4G). The gene discussed is PLVAP; the disease is congenital secretory chloride diarrhea 1.