Interestingly, even in GIST lacking WT KIT, anti-KIT antibodies inhibited tumor growth with an efficacy similar to what we observed in GIST-T1 cells following KITLG immunoneutralization, although the former effect was attributed to increased phagocytosis and stimulation of KIT degradation rather than prevention of KITLG binding [59]. The gene discussed is KIT; the disease is neoplasm.