The seminal discovery of the expression of CD117 in GIST was a major breakthrough. In more than 80% of GIST, c-kit proto-oncogenes have gain-of-function mutations that cause constitutive activation of c-KIT protein, a receptor tyrosine kinase (RTK), leading to tumorigenesis and proliferation [14-16]. The gene discussed is KIT; the disease is gastrointestinal stromal tumor.