AXL and neoplasm: These include hemi- or homo-zygous deletion of the wild-type KIT allele [6], overexpression of focal adhesion kinase (FAK) [7] and insulin-like growth factor receptor I (IGF-1R) amplification [8], BRAF V600E mutation (5% GIST) [9] and RTK switch (loss of c-KIT and gain of MET/AXL) [10], etc. Recently, it was shown that FGFR-signaling in GISTs significantly attenuated anti-tumor effects of IM, thus providing the evidence about the cross-talk between KIT and FGFR playing an important role in IM resistance [11,12].