These include hemi- or homo-zygous deletion of the wild-type Kit allele [6], overexpression of focal adhesion kinase (FAK) [7], insulin-like growth factor receptor I (IGF-1R) amplification [8], BRAF V600E mutation (5% GIST) [9], an RTK switch (loss of c-Kit and gain of MET/AXL) [10,15], activation of FGFR signaling, which attenuates the effects of IM in GISTs [11,12], etc. The gene discussed is AXL; the disease is gastrointestinal stromal tumor.