In glioblastoma mouse models, acquired resistance to CSF1R inhibition with rebounds of TAM was found to be mediated by the release of insulin-like growth factor (IGF), its interaction with IGF-1 receptor (IGF1R) on tumor cells and activation of protumorigenic downstream signals, providing a rationale for combined blockade of CSF1R with IGF1R and tumor tyrosine kinases [169]. Here, IGF1R is linked to neoplasm.