KIT and schwannoma: In particular, MET has been recently identified as a driver and potential therapeutic target in human MPNSTs [79], Hsf1 has been shown to be overexpressed and required for ras pathway activation and MPNST development following Nf1 loss in mice [80], and inhibition of KIT and PDGFR impedes the proliferation of schwannoma and MPNST cell lines and the development of xenograft-derived plexiform neurofibromas [81]–[83].