Similarly, the increased expression of VEGF-A was observed in GIST T-1 cells transfected by siRNA KIT (Supplementary Figure S1), thereby illustrating the inhibition of KIT signaling in GIST as a driving force for the activation of compensatory mechanism via the overproduction of VEGF-A and the activation of the VEGFR-mediated pathway. The gene discussed is KIT; the disease is gastrointestinal stromal tumor.