Using N-glycoprotein-capture mass spectrometry, Esposito et al. identified CD44 as the top candidate substrate of human Fut enzymes in MDA-MB-231 and SUM159-M1a breast cancer cells.216 However, a CRISPR/Cas9 CD44 knockout in BM2 cells did not decrease E-selectin binding in vitro or inhibit bone metastasis in vivo, implying that murine models of bone metastasis may not be E-selectin dependent. This evidence concerns the gene SELE and breast carcinoma.