Because we found that 1 μM CP-55,940 increases ERK1/2 signaling in CB1-low DBT cells without affecting the AKT, JNK, p38 and GSKβ signaling pathways, and one study suggested that ERK1/2 mediates the apoptotic properties of cannabinoids on astrocytomas [8], we then tested if inhibiting ERK signaling would affect the CB1-mediated and the cannabinoid receptor-independent killing of DBT cells. This evidence concerns the gene AKT1 and astrocytoma (excluding glioblastoma).