Anatomical and histopathological study of the developmental malformation in two cases of D1(13–15) trisomy has shown that a relation appears to exist between the additional chromosome and the malformations which characterize this trisomy. The excess chromosomal material appears to be directly responsible for the duplications (kidneys, Müllerian duct derivatives, fingers and toes) and excess tissue (supernumerary lobulations of liver, pancreas, lungs and kidneys) frequently found in this trisomy. The induced excess tissue may be basically abnormal or it may provoke an imbalance between it and the surrounding normal tissue, resulting in focal morphologic abnormalities in the structure of the tissue (liver, pancreas, kidneys). In addition, there are malformations (e.g. the skeletal abnormalities of the skull and face) which are better interpreted as the result of a series of secondary anomalies which had their origin in alterations occurring early in embryonic life. The cytogenetic disturbance responsible for the trisomy is better explained as a postzygotic nondisjunction, one daughter cell receiving 45 chromosomes. The presence of the additional chromosome in the surviving cell may explain the frequent occurrence of “situs inversus solitus” in this trisomy, a phenomenon known to occur in association with monozygous tw