Following on from this, it was shown that overexpression of the cyclin F mutant S621G led to an increase in the insoluble fraction of SFPQ and disrupted its subcellular distribution [84]; thus, cyclin F mutations could lead to dysregulation of SFPQ’s influence on RNA metabolism, which contributes to the pathomechanisms of ALS/FTD. This evidence concerns the gene CCNF and amyotrophic lateral sclerosis.