Mechanistically, tumor-expressed LILRBs drive key oncogenic functions, including proliferation, migration, angiogenesis, and metastasis, through activation of multiple pathways such as SHP2/calcium/calmodulin-dependent protein kinase 1 (CaMK1) 72, 223, 228, PI3K/AKT 224, 229, MAPK/ERK 230, 231, NF-kB 230, 232, 233, and JAK/STAT 118, 197 (Figure 2B). This evidence concerns the gene CAMK1 and neoplasm.