The interaction of ILT3 with ApoE can recruit SH2 domain-containing phosphatase two and Src homology two domain-containing inositol phosphatase 1(SHP2/SHIP1), which activates ERK1/2 to enhance tumor cell invasion and migration via facilitating epithelial-mesenchymal transition (EMT), and induce tumor angiogenesis via increasing the production of vascular endothelial growth factor A (VEGF-A), respectively (Li et al., 2021a). The gene discussed is LILRB4; the disease is neoplasm.