It has been more than thirty years since I first examined the propositus of the accompanying paper. My coauthors and I visited patient homes, neighboring states, church archives, and graveyards attempting to establish the inheritance pattern of the syndrome, which is now known as Kennedy disease. The pattern became certain 15 years later when a patient's half-brother by a different father developed the syn-drome. Today the question of diagnosis is answered by examining the X chromosome and finding expanded cytosine, adenosine, and guanine (CAG) repeats encoding a polyglutamine tract of the androgen receptor protein, similar to CAG repeats of four other degenerative diseases of late onset that affect specific cell types. Generally, a longer sequence predicts earlier onset. This genetic defect could result in a toxic effect rather than deficiency of product, and might be more amenable to therapy. Regardless, our work as neurologists is unfinished. Diagnosis is less difficult than the task that remains. Results of attempts to correct the genetic defect will not produce immediate benefit, leaving the neurologist the task of detecting whether therapy either stopped progression or bestowed some improvement on the patient's disordered motor, sensory, and endocrine systems. Most patients would settle for arrest of progression, allowing them to maintain their present level of fundion. They and we would rejoice if there were even minimal return of function.