Our results showing that CD57+ T-cells are mainly expanded in CMV-seropositive individuals, and maintain cytokine production and polyfunctionality independently of age, suggest that CD57+ T-cells may contribute to the promotion of adverse inflammatory outcomes, such as late graft dysfunction, chronic kidney rejection, cancer, and atherosclerosis observed after kidney transplant associated with CMV infection. The gene discussed is B3GAT1; the disease is atherosclerosis.