Of interest in this context is a recent study by Quail et al. (36), who found that in a transgenic mouse model of spontaneous GBM, cells that were dormant following colony stimulating factor receptor 1 (CSF-1R) inhibition became resistant to the treatment and were rescued from the dormant state by stroma-derived IGF-I, adding support for the role of IGF signaling in maintaining the balance between tumor cell proliferation, death and the acquisition of a dormant state. This evidence concerns the gene CSF1R and glioblastoma.