The broader Siglec–ligand network facilitates immune evasion through multiple tumor-specific mechanisms: (1) CD24-Siglec-10 interactions inhibit phagocytosis in ovarian/breast cancers [120]; (2) SELPLG engages Siglec-7 to promote myeloma immune escape [9]; (3) MUC1/MUC16 O-glycans bind Siglec-9 on monocytes/macrophages in breast cancer [115,121]; and (4) GD3 ganglioside suppresses NK cytotoxicity via Siglec-7 in melanoma [122]. Here, MUC16 is linked to neoplasm.