DBI and Alzheimer disease: Based on statistics performed by those authors, several proteins, including CLU, CALR, APOE, POSTN, HEXB, DB1, GFAP, HDGF, PRDX1, S10A9, CTSD, and SNX6, were all upregulated in AD, while VGF, BDNF, and GPM6A were downregulated, similar to our results on single excitatory human AD hiPSC‐neurons.[77] Another study by Johnson et al.,[78] which analyzed human AD brains and CSF samples, indicated that GFAP, CLU, APOE, DBI, CALR, PRDX1, CTSD, and AATM/GOT2 were upregulated, while VGF and GPM6A were downregulated,[78] again reminiscent of our findings on single excitatory human AD hiPSC‐neurons.