Here, we hypothesize that deletion of St3gal5 may offer a relief from downstream ganglioside-mediated immunosuppression, since tumor-associated gangliosides such as GM3, and GD3, are known to mask antigens,2 control the TCR repertoire,3 inhibit Fc receptor expression on monocytes and macrophages, leading to suppressed cytotoxicity, by promoting Treg development, and dampening dendritic cell activity. Here, ST3GAL5 is linked to neoplasm.