In an opposite fashion, B3GALNT2 appears to act in breast cancer in a secreted, N-glycosylated form by indirectly promoting FGF2-elicited angiogenesis mediated by GnT-Va [118, 162], and in hepatic cancer (uncharacterized whether N-glycosylated) by indirectly increasing the activity of macrophage migration inhibitory factor (MIF), a proinflammatory cytokine [117]. This evidence concerns the gene B3GALNT2 and breast carcinoma.