For instance, a Drosophila model of glioblastoma established by co-activating Epidermal Growth Factor Receptor (EGFR) and Phosphatidylinositol-3-Kinase (PI3K) pathways—commonly observed cancer driver alterations in these tumors—in glial cells and their precursors [18,19] can be used to test potential roles of other mutated genes observed in sequenced glioblastoma tumors in a genetic modifier screen. Here, EGFR is linked to glioblastoma.