Patients with amyotrophic lateral sclerosis/frontotemporal dementia due to ANXA11 mutations develop hallmark pathological features of TDP-43 mislocalization, including its loss in the nucleus and aggregation in the cytoplasm.8,30 We evaluated our P93S and wildtype ANXA11-expressing iPSC-derived neurons for evidence of TDP-43 related changes using immunocytochemistry (Fig. 4A). The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.