To explore this paradox, recent studies have forced the overexpression of ST6Gal-I in SW48 cells (a colon epithelial cell line deficient in both α2,3- and α2,6-sialyltransferases) and examined the effects of recombinant Gal-3 exposure on apoptosis (208) and their results demonstrate that ST6Gal-I-mediated α2,6-sialylation provides a survival advantage to tumor cells by inhibiting Gal-3-induced apoptosis, underscoring the enzyme’s role in tumor progression and resistance to immune-mediated cell death. This evidence concerns the gene LGALS3 and neoplasm.