In fact, α2,6 sialylation is a key mechanism for polarizing T cells helper 2 responses [8], reprogramming tumor-associated endothelial cells [9] and rewiring the function of myeloid-derived suppressor cells [51] by modulating sensitivity to Galectin-1, which promotes immunosuppression, angiogenesis and metastasis through binding to different glycosylated receptors, including integrins [52]. Here, LGALS1 is linked to neoplasm.