NF1 and glioblastoma: Furthermore, since the loss of NF1 in glial cells has been found to be associated with increased RAS activity, targeting the RAS-downstream signaling pathways (e.g., the RAF-MEK-ERK signaling cascade) through MEK inhibition may be another viable therapeutic strategy to prevent NF1-associated mesenchymal transformation in GBM [17, 57, 78].