Of particular note is that while agonizing CD137 has shown benefits in reducing the pathogenic autoantibodies and lymphocytes and amelioration of clinical manifestation of SLE in animal models, a number of in vitro studies using nonlupus human samples have revealed that CD137 activation enhances ingression of monocytes and their interaction with ICAM-1 in blood vessels, leading to atherosclerosis and plaque inflammation which may potentially amplify cardiovascular risk [66–68]. The gene discussed is TNFRSF9; the disease is systemic lupus erythematosus.