Given the detrimental effects of NLK overexpression on nucleocytoplasmic transport (Figures 1–9) and neuron survival (Figure 10), and the elevated NLK mRNA and protein observed in patients and disease models (Figure 11), we asked whether targeting NLK could ameliorate disease phenotypes in ALS/FTLD-TDP models. Here, NLK is linked to amyotrophic lateral sclerosis.