Finally, (iii) Alzheimer’s disease (AD) pathogenesis has been studied using cerebral organoids originating from patient-derived iPSCs carrying familial mutations of AD [38], iPSC transfected with an episomal plasmid vector to introduce mutated Tau protein (P301S) [39], or iPSC chemically induced by Aftin-5 to secrete Aβ42 peptide [40]. This evidence concerns the gene MAPT and Alzheimer disease.