To determine cellular interactions during GBM progression, we leveraged our de novo GBM mouse model2–4 wherein tumors are initiated in situ from conditional (Cre/Lox) overexpression of human EGFR combined with loss of Cdkn2a and Pten. A conditional luciferase reporter gene8 was used for monitoring GBM growth by bioluminescent imaging (BLI). The gene discussed is CDKN2A; the disease is glioblastoma.