These include hemi- or homozygous deletion of the wild type Kit allele [13], BRAF V600E mutation (5% GIST) [14], a RTK switch (loss of c-Kit and gain of AXL) [1], over-expression of focal adhesion kinase (FAK) [15] and insulin like growth factor receptor I (IGF-1R) amplification [16]. This evidence concerns the gene AXL and gastrointestinal stromal tumor.