The research found that VEGF/Notch signaling pathways mediate an immunosuppressive onco-fetal TME in HCC.450 Further investigation revealed a common immunosuppressive microenvironment between fetal liver and HCC, particularly involving VEGF/Notch signaling in the re-emergence of fetal-associated endothelial cells (i.e., PLVAP/VEGFR2) and fetal-like (i.e., FOLR2) tumor-associated macrophages.451 This concept of an immunosuppressive onco-fetal TME mediated by VEGF/Notch signaling provides a potential new target for immunotherapy of HCC. Here, FOLR2 is linked to hepatocellular carcinoma.