found that VEGFA secreted by proliferative hepatocytes induced the re-emergence of fetal-like PLVAP+ endothelial cells via directly regulating PLVAP expression, which, in turn, reprogrammed immunosuppressive fetal-like FOLR2+ tumor-associated macrophages (TAMs) via the DLL4/NOTCH2 signaling axis, thereby maintaining an immunosuppressive onco-fetal ecosystem in liver cancer (24). The gene discussed is PLVAP; the disease is neoplasm.