Previous studies have suggested that VEGF, secreted from hepatocytes in cell division, could regulate the re-emergence of fetal-like PLVAP+ endothelial cells, which, in turn, reprogramed immunosuppressive fetal-like FOLR2+ TAMs via the DLL4/NOTCH2 signaling axis, thereby maintaining an immunosuppressive onco-fetal ecosystem in HCC (24). Here, PLVAP is linked to hepatocellular carcinoma.