Possibly the “state” of Ndst1 deficient APCs (DCs and/or macrophages) in tumors, including cytokines produced, or the maturational state of such cells (e.g., elevated CD80/86, MHCII expression, as noted in [1]) may activate certain signaling pathways that drive Ndst1 deficient APCs away from the typically tolerogenic state induced by the early cancer microenvironment. This evidence concerns the gene CD80 and cancer.