VGF and BDNF are known to be neuroprotective neurotrophic factor pathways that are downregulated in postmortem human AD brains and thus have been implicated in AD pathogenesis.[27, 28] The next most downregulated protein in the AD hiPSC‐neurons was DNJC8 (or heat shock chaperone HSC70), whose modulation has been proposed as a therapeutic for AD because chaperones can be used to refold aggregated proteins.[29] However, to our knowledge, this is the first report of specific downregulation of a chaperone in excitatory neurons in AD. Here, VGF is linked to Alzheimer disease.