LFA is expressed on neutrophil membranes and the MAC-1 glycoprotein complex is retained in secondary granules.[4] LFA-1 has been shown to be involved in the initiation of insulitis in humans and animal models of type 1 diabetes.[38,39] Treatment with monoclonal antibodies against LFA-1 can delay the spontaneous onset of the disease in NOD mice.[40–43]. The gene discussed is ITGAL; the disease is type 1 diabetes mellitus.