TDP-43 functions mainly in the nucleus, and its redistribution from the nucleus to the cytoplasm has been recognized as a pathologic hallmark of ALS and FTLD, suggesting that the pathogenic mechanism is associated with the loss of nuclear TDP-43 function (Mackenzie et al., 2010; G. Kim et al., 2020). This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.