In GIST, mutations in the kinase domain of KIT are usually due to secondary point mutations (Kitamura and Hirotab, 2004) and can confer resistance to imatinib due to the altered conformation of the kinase which prevents drug interaction with the ATP binding pocket (Frost et al, 2002; Foster et al, 2004). This evidence concerns the gene KIT and gastrointestinal stromal tumor.