Neurofibromas are PNS tumours derived from de-differentiated Schwann cells, driven by loss-of-function mutations in the NF1 tumour suppressor gene and subsequent Ras hyperactivation. This genetic defect renders Schwann cells more susceptible to tumourigenic transformation, but additional signaling from the injured nerve microenvironment is required for tumour formation. Using both in vivo and in vitro models, my research focuses on the identification and characterisation of microenvironmental factors that synergise with NF1 loss to induce tumourigenic reprogramming of Schwann cells.