The creation of this dual model serves to demonstrate the ease with which knockdown can be combined with established neurodegenerative disease models and will allow us to evaluate if Stmn2 deficiency in the presence of the expanded C9ORF72 repeat and endogenous Tdp-43 pathology exacerbates pathology, thereby providing a more complete model of FTD. This evidence concerns the gene STMN2 and frontotemporal dementia.