Interestingly, loss of SEMA4A alone in monocytes was sufficient to reduce the size of heterotypic PLXNB2+ tumor clusters which is comparable with the effects of PB2 KO in tumor cells, suggesting that SEMA4A is the primary ligand on monocytes for PLXNB2-dependent tumor-monocyte clustering (Fig. 5a). This evidence concerns the gene SEMA4A and neoplasm.