Present evidence for the genetic basis of “acquired” agarnmaglobulinernia has been reviewed. The previously demonstrated serologic abnormalities and the quantitative abnormalities ofin vitrolymphocyte response to phytornitogens in parents of these patients are reported. In addition, a qualitative difference in the resultant cell types followingin vitrostimulation of lymphocytes with pokeweed mitogen (PWM) between agammaglobulinemic patients, their parents, and normal individuals has been shown. These studies suggest that “acquired” agammaglobulinernia is an autosomal recessive disease, perhaps related to either a defective lymphocyte subpopulation or failure of cytodifferen