Though the monoclonal antibody for ICAM-1 (enlimomab) successfully improved neurological functions with reduced lesion size by reducing cerebral neutrophil influx in ischemic stroke models of rat and rabbit (Zhang et al., 1994; Bowes et al., 1995), it has no beneficial effect in ischemic stroke patients, instead, it induced significantly worse outcomes (Enlimomab Acute Stroke Trial, 2001), suggesting the roles of cerebral neutrophil infiltration might vary in different species upon ischemia/hypoxia. The gene discussed is ICAM1; the disease is ischemic stroke.