LILRB4 and neoplasm: In NSCLC, LILRB4 recruits SHP-2 and SHP-1, which results in subsequent ERK1/2 signaling activation, mediating the epithelial–mesenchymal transition (EMT) and increasing vascular endothelial growth factor (VEGF-A) expression in NSCLC cells in support of tumor cell invasion and angiogenesis [112].