We have previously shown that human iPSC‐derived cortical neurons with the 10+16 MAPT mutation linked to FTD exhibit pathophysiological excitability at late stages of neurogenesis (≈150 DIV), revealed as a depolarized resting membrane potential associated with impaired firing due to reduced expression of Nav1.6 channels.24 The gene discussed is MAPT; the disease is frontotemporal dementia.