Gastrointestinal stromal tumour(GIST) is a tumour of mesenchymal origin and accounts for the majority of mesenchymal tumour of gastrointestinal tract. Its incidence is evaluated between 7 to 15 cases per 1 million persons per year. The most common mutation in GIST is the gain-of-function mutation of the KIT and gain-of-function mutation of the platelet-derived growth factor (PDGF) receptor alpha (PDGFRA). The relative frequency of KIT mutation is around 80% whereas the relative frequency of PDGFRA is between 5-8%. However, around 12-15% of GIST tumours are both KIT and PDGFRA wild-type. There is a high need to better understand the molecular drivers for GIST tumours in general and KIT and PDGFRA wild-type GIST tumours in particular. In order to better understand, KIT and PDGFRA wild-type GIST, we aim to produce a genetically engineered mouse model of GIST driven by BRAF and PI3K mutations. To do so, we have crossed mice expressing a tamoxifen dependent Cre-recombinase ERT2 under a glial-cell specific promoter (Glial fibrillary acidic protein or GFAP) with BrafCA/CA;Pik3caLat/Lat. The resulting mice when injected with tamoxifen give rise to GIST in mice. Our aim is now to better understand and characterise the development of GIST in this model.