The efficiency of tumorigenesis was even higher upon synchronous Nf1 loss, conveying indirect activation of RAS/MAPK signaling (Fig. 2c), typically observed in patients suffering from Neurofibromatosis Type 1 (NF-1), who exhibit an increased risk for malignant peripheral nerve sheath tumors (MPNST) or Nf1-deleted eRMS37. This evidence concerns the gene NF1 and neurofibromatosis.