Previously, we and others found a hyperexcitability phenotype in AD hiPSC‐derived cerebrocortical neurons (AD hiPSC‐neurons) bearing either amyloid precursor protein (APP) or presenilin 1 (PS1) patient mutations compared to isogenic, gene‐corrected wild‐type (WT) control neurons.[13, 14] In fact, this excessive electrical activity resembled that seen in human AD brains on electroencephalograms (EEGs) in several respects,[1, 2, 3, 4, 13, 14] suggesting that AD hiPSC‐neurons represent a model system for at least that aspect of the disease. Here, APP is linked to Alzheimer disease.