Notably, the ability of S1, S5, and S6 for Siglec-15 to disrupt interactions with key ligands (CD44, MAG, sialyl-Tn, and LRR4C) suggests a dual mechanism of action: direct blockade of Siglec-15-mediated immunosuppressive signaling and potential modulation of ligand-dependent tumor-stroma crosstalk. This evidence concerns the gene MAG and neoplasm.