To examine whether APC deletion in GFAP-Cre; KrasG12D; p53L/L compound mice drives GBM formation in vivo, we usually compare phenotypic differences in gross appearance, behavior, and pathohistology between GFAP-Cre; P53L/L, GFAP-Cre; KrasG12D; p53L/L, and GFAP-Cre; KrasG12D; APCL/+; p53L/L mice. The gene discussed is APC; the disease is glioblastoma.