Since human express functional RPA4 and produce Alt-RPA but mice do not [39,40,42], the presence and absence of Alt-RPA may play a role in the different requirements of CAG repeat numbers for Huntington’s disease onset in these two organisms, possibly by modulating somatic CAG repeat expansions that modulate the disease state (B. Lahue, personal communication). The gene discussed is RPA1; the disease is Huntington disease.