Recently, it has been demonstrated that unstable trinucleotide repeats are the etiologic factor in myotonic dystrophy, fragile-X syndrome, Kennedy's disease, Huntington's disease, spinocerebellar ataxia type 1, and dentatorubral-pallidoluysian atrophy. All available evidence suggests that these expanded trinucleotide repeats, or unstable DNA, are the biological basis of the clinical phenomenon of genetic anticipation. Two components of anticipation, increased severity and earlier age of onset in subsequent generations, have been widely observed in schizophrenia. We review the evidence for and against genetic anticipation in schizophrenia. Although the major criticisms of the anticipation hypothesis can be questioned, so can the evidence in favor of it. We conclude that molecular genetic approaches might be the most useful means of resolving ambiguity in clinical arguments about the origin of the anticipation-like phenomenon in schizophrenia.