Specifically, binding of CSF-1 to CSF-1R triggers auto-phosphorylation of the receptor on several tyrosine residues, and this can activate multiple intracellular pathways, including the phosphatidyl inositol 3-kinase (PI3K) pathway, which promotes macrophage maturation and upregulates expression of genes that lead to the pro-tumor M2 phenotype [1]. This evidence concerns the gene CSF1R and neoplasm.