Alterations of immune function can result not only from alcohol consumption by the adult human or animal, but also from fetal alcohol exposure (FAE). We have demonstrated long-lasting effects of FAE on T cell function and effects of adult ethanol (EtOH) consumption on tumorigenesis. Here, we present recent data that demonstrate that 1) FAE alters the biphasic pattern of thymocyte activation during peripubertal development probably due to effects other than the CD3 pathway; and 2) the long-lasting impaired proliferative response of splenocytes from FAE rats is not due to loss of their ability to express interleukin-2 receptors (IL2R), thus reflecting interference with events following the IL2-IL2R interaction. We also provide direct evidence that acute in vivo administration of EtOH to adult Fisher 344 rats can suppress blood natural killer (NK) cytotoxicity and that such suppression mediates the observed enhanced metastatic growth of a syngeneic mammary tumor.