If these variants do indeed prove to be involvedin the pathogenesis of synucleinopathies, they might be targeted fordisease treatments; for example, with RNA interference technology,which would be designed to target specific toxic isoforms of SNCA and facilitate cleavage of the relevant mRNA to preventit from being translated. This technologyhas already proved successful in reducing levels of another amyloidogenicprotein, transthyretin, in familial amyloid polyneuropathy. This evidence concerns the gene TTR and familial amyloid neuropathy.