In previous studies, the search for genetic modifiers in C9orf72 disease, as well as in many other diseases, has been mainly assessed using SNP-based genome-wide association studies which poorly tag potential signals of association coming from multi-allelic STRs.29 This is a significant limitation, particularly in studying genetic modifiers in FTD-ALS, given the well-established molecular and biological links between TDP-43 aggregation pathologies and diseases associated with CAG polyQ expansions. This evidence concerns the gene C9orf72 and frontotemporal dementia.