However, pharmacologically targeting Hedgehog/GLI signaling, decreasing KIT expression, and likely hitting Hedgehog-independent ATO targets (e.g., reactive oxygen species, phosphatase inhibition or JNK/AP-1 activation of redox-sensitive enzymes [39]) in GIST represents a novel approach to disrupting GIST dependence upon KIT signaling for survival, irrespective of imatinib-sensitive or imatinib-resistant KIT mutation status. Here, KIT is linked to gastrointestinal stromal tumor.