A GENETIC strain of ataxia was isolated from rabbits by Sawin and reported upon in detail by Sawin, et al.1 Anders2 described the histopathology of the brainstem lesions and this report was later amplified by O'Leary, et al3 in this journal. The condition results from the action of a lethal single recessive mutant gene. In the affected members of a litter, clinical manifestations and the characteristic lesions appear at adolescence so that with sufficient material it is possible to evaluate the chronology of lesions and relate their distribution and severity to the clinical state of the animal. Between the earlier and later pathological report (17 years), many generations of the strain intervening, the natural history became so altered that instead of the affected animals pursuing a fulminating course to death in two to three weeks, a significant number lived much longer. Thus, this later report provides a