Targeting PD-1 to enhance antiviral immunity may increase cardiovascular risks by activating proatherogenic T cell responses, including atherosclerosis.[125,126] The coexpression of PD-1 and Tim-3 on CD8 + T cells is upregulated in human atherosclerosis, and this T cell subset from the lesional arterial blood produces more anti-atherogenic cytokines. The gene discussed is HAVCR2; the disease is atherosclerosis.