The development of the cerebellum has been studied in normal and reeler mice, from embryonic day fourteen, i.e. when morphogenesis begins in this organ, to birth. The cerebellar nuclei develop according to a similar sequence in both genotypes. Their neurons migrate into the rostral field of the cerebellar bud where they condense in a rounded mass, well defined at E14. From E17, this cell contingent spreads transversally and the three roof nuclei become clearly defined. In reeler mutants, there seems to be an abnormal development of the architectonics of the lateral nucleus. The Purkinje cells migrate into the cortex at the same time in both genotypes. In the normal animal, from E14 onward, Purkinje cells are condensed in a clearly defined plate, where they assume a radial organization. By contrast, the mutant Purkinje cells are not arranged in a plate but are scattered in the periphery of the cortex. The neurons of the external granular layer are identical in both genotypes. Radial glial fibers and early Golgi epithelial cells appear to be normally present in the reeler embryo. The foliation of the cerebellar cortex begins at E17 in the normal embryo. From this stage onward, foliation is increasingly deficient in reeler mutants. Based on these observations, it is suggested that, in normal cerebellar development, a specific, genetically determined mechanism is responsible for the organization and the stabilization of postmigratory neurons and that this mechanism is affected by the reeler mutation.