In particular, activation of PI3K/Akt/mTOR pathway in GIST is due to the constitutive activation of c-KIT/PDGFRA autophosphorylation and involved in oncogenesis and tumor progression at various disease stages [1], and is also thought to be linked with GIST resistance to imatinib mesylate (IM) [2,3]. The gene discussed is AKT1; the disease is neoplasm.