Chromosome and enzyme markers have been studied in 21 benign ovarian teratomas from 14 patients. Markers heterozygous in the patient were completely homozygous in 52% of the teratomas and completely heterozygous in 19%. The remainder showed a mixture of the two, 10% having homozygous centromeres with some heterozygous enzyme markers and 19% having heterozygous centromeres and some homozygous enzyme markers. These results suggest that benign ovarian teratomas in the present series arise from germ cells in a number of different ways. Those with heterozygous centromeres probably arise by failure of meiosis I. Some tumours with homozygous centromeres must arise by failure of meiosis II, but because of the low level of heterozygous enzyme markers in this group a substantial number are thought to arise by duplication of a mature ovum to give an entirely homozygous genotype, genetically the female equivalent of the complete hydatidiform mole.