In the Ldlr-/- hyperlipidemia mouse model, whether it was LAG-3 deletion, LAG-3 monotherapy blockade, or LAG3/PD-1 dual-target inhibition, although it did not increase the plaque burden in Ldlr-/- mice, it increased the accumulation of CD4+ T cells in arterial plaques and the vascular adventitia, and expanded the populations of CD4+ and CD8+ effector T cells and Tregs in the spleen and peripheral blood circulation, along with increased IFN-y production. The gene discussed is LDLR; the disease is hyperlipidemia.