The NF1-p53 cell line was generated from a murine MPNST driven by loss of Trp53 and Nf1, with Met amplification occurring spontaneously, while the NF1-MET cell line was driven by amplification of Met in the context of Nf1 loss [34], with spontaneous deletion of Cdkn2a. We further used Crispr-Cas9 to generate a p53-deficient isogenic cell line, NF1-MET;sgP53, from the NF1-MET cells to identify p53-specific regulation of drug response. This evidence concerns the gene MET and malignant peripheral nerve sheath tumor.