Mechanistically, LILRB2 promoted CRC progression by interacting with HLA-G, activating AKT and ERK signaling (Figure 4A) 322, enhanced tumor angiogenesis via MAPK/ERK-mediated upregulation of vascular endothelial growth factor (VEGF)-A and fibroblast growth factor 1 (FGF-1, Figure 4A) 231. This evidence concerns the gene LILRB2 and neoplasm.