Consistent with these findings, recently, a feedback cycle between nucleocytoplasmic transport (NCT) defect and TDP-43 aggregation was proposed as a model to explain cytoplasmic accumulation of TDP-43 in ALS conditions (Solomon et al., 2018; Gasset-Rosa et al., 2019). The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.