The PD-1 regulation through CD69-oxLDL could contribute to the exacerbated phenotype observed in a previous atherosclerosis model in the bone marrow (BM) chimeric Ldlr−/− mice deficient for CD69 only in the lymphoid compartment and also in asymptomatic individuals with subclinical atherosclerosis (Tsilingiri et al., 2019[81]). This evidence concerns the gene PDCD1 and atherosclerosis.