Given that other cyclin F mutations were also discovered and potentially linked to both sporadic and familial ALS and FTD in our previous GWAS study (Williams et al., 2016), we wanted to develop a relatively high-throughput, quick and informative strategy that could screen additional CCNF mutations (K97R, S195R, S509P and R574Q) to determine whether i) they were disease-causing and therefore used as model systems, and ii) verified by other biochemical and in vivo studies. This evidence concerns the gene CCNF and frontotemporal dementia.