At the molecular level, 85–90% of GISTs possess mutually exclusive gain-of-function mutations in KIT or in the related RTK PDGFRA (Hirota et al., 1998, 2003; Rubin et al., 2001; Heinrich et al., 2003), while ∼10–15% lack these kinase mutations and are known as wild type (WT) GIST. Here, PDGFRA is linked to gastrointestinal stromal tumor.