However, in an another RCAS-hPDGF-B inducible glioma model, Quail et al. found that although CSF-1R inhibition resulted in tumor shrinkage, secretion of IGF-1 in TAMs, and upregulation of IGF-1R in tumor cells resulted in activation of the PI3K pathway in glioma cells, stimulating tumor rebound growth, and recurrence (86). This evidence concerns the gene CSF1R and neoplasm.