In systemic lupus erythematosus (SLE), diabetes, and rheumatoid arthritis (RA), this is regulated by inhibition of galectin-mediated immunosuppressive prevention of ICAM-1/LFA-1 interaction (50), aberrant expression of ICAM-1 N-glycans due to high glucose (51), and activity of glycosyltransferases (52). This evidence concerns the gene ICAM1 and systemic lupus erythematosus.