CCL5 and glioblastoma: Since the NF1 protein, neurofibromin, functions as a negative regulator of RAS, specifically K-RAS in astroglial cells [13, 14], and NF1 mutation/loss characterizes the mesenchymal GBM (M-GBM) molecular subtype [15], we sought to determine whether Ccl5 expression creates a unique autocrine circuit for mesenchymal glioblastoma growth.