The albino rats used in this study were obtained originally from the Wistar Institute of Philadelphia and belong to a strain in which microphthalmia was first observed by Dr Helen Dean King in the F4 generation extracted from a cross between an albino female of this stock and a wild grey Norway male. The defect occurred only in the “S” strain which formed a small proportion of the main stock. Its inheritance was observed by King (1931) through eleven generations, and 538 rats having either both or a single eye microphthalmic were obtained in a strain comprising 1884 individuals. The greater frequency of microphthalmia in the American stock is a marked feature, since only 154 rats with eye defects have been observed in the Edinburgh branch of Wistar rats in fourteen generations comprising over 5000 rats, and this total includes animals with eyes of normal size but possessing defects such as aniridia, cataract, etc., and also rare cases of anophthalmia and buthalmos. It is probable that 80 per cent, of the total affected were microphthalmics, and apparently the defect was generally more pronounced than in the parent stock, that is if the rat illustrated in King's monograph is to be taken as typical. According to King, the eye-defect could easily be detected at birth, “since a small eye did not protrude from the socket.” In the total given here no still-borns are included, as it was found that this method of diagnosis, as also the opacity of the lens in such rats immediately or soon after birth, were unreliable criteria of abnormality. We are in agreement that prenatal mortality did not play an important role in determining the ratio of normal to abnormal individuals, because litters containing affected were of the average litter size and generally contained some normals (Table I). However, where a large number of still-born rats occurred in litters containing defectives, it is possible that the abnormality involved proved lethal, since still-births are not of common occurrence in this stock (Table II).