Hypersialylation can drive cancer progression by mediating the stability of cell surface receptors on cancer cells and integrin-mediated interactions and enhancing immune evasion by engaging sialic acid-binding immunoglobulin-like lectin (Siglec) receptors on immune cells, modulating antigen presentation, interacting with selectin receptors and modulating the stability of surface proteins on immune cells [2–4]. Here, CD177 is linked to cancer.