The pathogenesis of anorectal malformations was studied in 41 abnormal embryos, foetuses and newborn pigs descended from a herd in which this anomaly was caused by a hereditary trait. The principal development error was found to be situated in the cloacal plate, of which a dorsal part of variable size was missing. This defect impeded the normal migration of the dorsal cloaca and adjacent structures along the dorsal border of the plate to the body surface of the tailgroove. Correlated to the size of the cloacal plate defect diverse types of anorectal malformations may develop ranging from slight abnormalities such as anal stenosis and perineal or vulvar ectopic anus to more serious anomalies such as imperforate anus of low, intermediate and high types. In the cases with imperforate anus a communication with the urogenital system is always formed, although it may disappear later in some animals. This communication which represents a persistent cloaca, has to be considered as an ectopic anorectal canal according to its origin and structure. The abnormalities of the internal and external sphincter ani muscles and puborectal muscles are secondary although distinctly correlated to the malformations of the epithelial structures.