Analysis of several inbred strains of rabbits with high ( 3 0 5 0 % ) frequencies of accessory spleens revealed that hereditary hematological diseases, autoimmune hemolytic anemia and lymphosarcoma, occurred in some of them. Twenty-one per cent of individuals in these strains, though phenotypically normal, had globulin-coated (Coombs'-positive) erythrocytes. These findings supported observations of increased frequency of accessory spleens in human beings with similar diseases (e.g., autoimmune hemolytic anemia, idiopathic thrombocytopenic purpura, "secondary hypersplenism," Gaucher's disease, hereditary spherocytosis, etc.) and suggested that accessory spleens represent physiological responses to demand for phagocytic capacity provided by the reticuloendothelial system in the spleen, rather than as passive developmental anomalies. This hypothesis predicted that simulation of the basic defect might yield a laboratory model for the induction and study of accessory spleens in rabbits. Phenylhydrazine was used for this purpose and it was shown that the frequency of accessory spleens