We showed previously that inhibition of KIT signaling in GISTs activates FGFR-signaling pathway rendering cancer cells resistant to receptor tyrosine kinase inhibitor (RTKi) imatinib mesylate (IM) (Gleevec) despite of absence of secondary <i>KIT</i> mutations and thereby illustrating a rationale for the combined (e.g., KIT- and FGFR-targeted) therapies. Here, KIT is linked to cancer.