Subsequently, the soluble/insoluble and total protein level of sumoylated and un-sumoylated proteins were also examined, both bands of soluble and insoluble fraction of ataxin-3-68Q were denser than those of ataxin-3-68QK166R indicating the SUMOylation modification of mutant-type ataxin-3 might enhance the stability of the protein and participate in the pathogenesis process of SCA3/MJD to a certain degree. This evidence concerns the gene ATXN3 and Spinocerebellar ataxia type 3.