IN RECENT years there has been increased interest in familial and acquired anemias associated with erythrocytic inclusion bodies.<sup>1</sup>Simultaneously, the hereditary transmission of certain hematological disorders has received attention.<sup>2</sup>The purpose of this report is to present an investigation which has led us to propose that there exists a type of hemolytic anemia secondary to a hereditary defect in hemoglobin synthesis and associated with rubricytic inclusion bodies. It is our opinion that mechanisms heretofore not generally recognized have been demonstrated in this study. <h3>BACKGROUND</h3><h3>A. Familial Anemias.</h3> —The familial nature of certain anemias is well known. Familial hemolytic anemia (familial spherocytosis) is transmitted as a mendelian dominant trait, and the genetics of hereditary leptocytosis (thalassemia; Mediterranean disease) and sickle cell disease have been clarified recently. Valentine and Neel<sup>2e</sup>postulated that thalassemia major may be due to homozygosity for a factor which when