Taken together, these findings suggest a model in which disease-associated LCD mutations or nuclear import defects cause increased cytoplasmic concentration of FUS and augment its recruitment to stress granules, which over time develop into pathological inclusions, potentially due to increased FUS self-interactions or misfolding (Bentmann et al., 2013; Lin Y. et al., 2015; Molliex et al., 2015; Patel et al., 2015). Here, FUS is linked to lattice corneal dystrophy type I.