When the LDLR-deficient mouse was also knocked out for both PD-L1 and PD-L2 genes, it led to: (i) an infiltration of increased numbers of lesional CD4+ and CD8+ T cells and macrophages; (ii) a burden of atherosclerosis throughout the aorta; (iii) elevated serum levels of TNF-α; (iv) highly potent APCs as T cell stimulators [115], indicating dysregulated systemic T cell responses for the development of arterial diseases [116]. This evidence concerns the gene PDCD1LG2 and atherosclerosis.