**9. Conclusions**

Significant research e fforts over the past three decades have significantly advanced the state of knowledge of the genetic landscape of human MPNST. Particularly in NF1-associated MPNST, it is generally accepted that alterations in *NF1*, *CDKN2A*, *TP53*, and *SUZ12* are involved in tumor progression from benign to malignant tumors. However, less frequent alterations in genes with complementary function have been described in subsets of tumors, and additional tumor-driving mutations may be present in sporadic or recurrent/metastatic tumor samples. Future genomic studies should aim to incorporate as many well-annotated samples as feasible and clearly report on di fferences between NF1-associated and sporadic MPNST subtypes. Exciting future work will also incorporate additional technologies to improve our understanding of the downstream consequences of genomic alterations for MPNST biology and aid in development of improved treatments.

**Author Contributions:** All authors researched the published literature, conceived, wrote, and edited the manuscript. All authors have read and agreed to the published version of the manuscript.

**Funding:** K.M.L. is supported by a Young Investigator Award from CureSearch for Childrens Cancer. C.A.P. receives research funding from the Neurofibromatosis Therapeutic Acceleration Program (NTAP).

**Conflicts of Interest:** The authors have no conflicts of interest to declare, with the exception of Christine A. Pratilas, who served as a co-editor for this special issue of Genes. Christine Pratilas has abstained from editorial duties relating to this manuscript. Christine A. Pratilas is a paid consultant for Genentech/ Roche.
