Regarding the immunological mechanisms of LAG3 in T cells, a study using a mouse model of type 1 diabetes demonstrated that, in the absence of the co-inhibitory receptor PD-1, LAG3 expression may promote the differentiation of islet CD8 + T cells from naïve to suppressive or even terminally differentiated states, limiting epitope spreading and interfering with antigen recognition to dampen immune responses [28]. This evidence concerns the gene CD8A and type 1 diabetes mellitus.