This view is supported by the finding that the binding of Gal-1 to SLE T cells, an anti-inflammatory human lectin, decreases because of the different sialylation of SLE T cells from that of healthy T cells, and thus it must be another reason that SLE T cells are more resistant to Gal-1-induced apoptosis [20]. The gene discussed is LGALS1; the disease is systemic lupus erythematosus.