Inhibition of N-linked glycosylation of KIT has been reported to affect cellular signaling and cell-surface expression of KIT, inducing apoptosis in acute myeloid leukemia (AML)65, and glucose metabolism mediated by KIT in response to imatinib has been used to predict tumor sensitivity to the drug in gastrointestinal stromal tumors (GIST)66. Here, KIT is linked to neoplasm.