Anti-VEGF-A refractory tumors enhanced galectin-1 secretion together with its increased binding to neovascular endothelial cells due to altered glycosylation patterns (i.e., decreased α2,6-linked sialic acid) on VEGFR2, leading to galectin-1-driven angiogenesis and tumor progression. The gene discussed is KDR; the disease is neoplasm.