Abrogation of l-fuc-induced itIC and tumor growth suppression by EB1 knockdown was rescued by reconstitution with only WT but not glycofucomutant EB1, demonstrating that glycosylation–fucosylation of EB1 or HLA-DRB1 is essential for l-fuc-triggered itIC induction and melanoma suppression (Fig. 4f and Extended Data Fig. 5f,g). The gene discussed is HLA-DRB1; the disease is melanoma.