Since we found that KPNB1 is abnormally sequestered into pTDP-43 inclusions in ALS/FTD patient tissue, we conclude that increasing expression or activity of KPNB1 may be therapeutical in restoring normal localization and function of TDP-43, thus mitigating neurodegeneration. This evidence concerns the gene KPNB1 and frontotemporal dementia.