Molecular subtyping of GIST is an important factor for both prognosis and estimation of response to TKIs.31 Wild-type GIST is considered resistant to imatinib and is associated with different alterations, such as succinate dehydrogenase deficiency and neurofibromatosis type 1 or Ras–mitogen-activated protein kinase pathway alterations, among others.32,33. The gene discussed is WNK2; the disease is gastrointestinal stromal tumor.