Evidence, based on five series of mouse-human somatic cell hybrid clones, is presented for assignment of a human gene for adenosine deaminase (ADA: EC 3.5.4.4) to chromosome 20. The human form of adenosine deaminase expressed by the hybrid cells apeared to be identical to the isozyme found in erythrocytes, judging from its electrophoretic mobility and reactions with p-chloromercuribenzoic acid (PCMB). Absence of ADA activity has been associated with a combined immunodeficiency syndrome. The relationship of our data to hypotheses concerning this association is discussed.