Given that ST6Gal I and α2,3 sialyltransferases share common substrates and overexpression of ST6Gal I could lead to the decrease in α2,3 sialylation through substrate competition mechanisms [67], it is reasonable to hypothesize that the inhibitory effects of ST6Gal I overexpression on tumor growth is the direct result of decreased α2,3 sialylation. The gene discussed is ST6GAL1; the disease is neoplasm.