10, 11, 12, 13, 14 Previous researches demonstrated that extracellular Aβ or phosphorylated tau‐induced impairment of synapses,15 disturbed mitochondrial dynamics16, 17, 18, 19 and defective autophagy system,20, 21, 22 and these compounding features of AD cannot be represented easily in other cellular model systems than iPSC system. Moreover, iPSC‐based disease modelling has the great potential towards personalized treatment as each iPSC line is patient‐specific and the response of drug treatments can be accurately monitored prior to human treatment.7, 10. This evidence concerns the gene MAPT and Alzheimer disease.