The Frem2my mutation was identified in the early 1920s in offspring of irradiated grandparents. What is known of the mice that were irradiated is that they were of "a stock of colored animals that had been inbred for several years and hence was in a fairly homogeneous condition" that they "were obtained from Mrs. Gray, successor to A.E.C. Lathrop" (Bagg and Little,1924), and that the two irradiated founders of this line were both brown (Little and Bagg, 1923). Irradiated female #85 was bred to irradiated male #49, their offspring were sibling mated, and their inbred descendants are line 85. 17 mice in the F3 generation from these irradiated parents showed the most consistent deviant phenotype of Frem2my, eye abnormalities. In 1950 K.P. Hummel at The Jackson Laboratory reported breeding a C57BL/cdJ female to an F71 male from "line 85" which she had received from E.C. MacDowell in 1948 (Hummel, 1950). In 1951 she reported outcrossing an F8 male to a female C3H/Hu (later updated to C3HeB/HuJ by J. Staats, 1968). The F2 from this outcross were then bred to produce a line that was homozygous for a, Tyrpb, and Frem2my (Humel, 1951). In 1968 this homozygous inbred strain, called MY/Hu, was at F31 and has been maintained by sibling breeding since that time. In 1973 it was passed to Priscilla Lane at The Jackson Laboratory where it continued to be maintained by sibling breeding. Isoenzyme profiles in 1983 showed Pep3c and Car2a alleles in MY/HuLe which are distinct from both C3H and C57BR/cdJ profiles, while the other isoenzymes assayed are held in common with either C3H, C57BR/cdJ, or both. MY/HuLe embryos were frozen in 1988 and 1989 by sibling mating at F107 and beyond.