The earliest models of human‐derived AD pathogenesis used iPSCs from patients with sporadic AD, familial AD,67 or Down's syndrome68 that differentiated neurons in 2D, but later studies showed that 3D models of familial AD were able to more accurately model Aβ and tau pathology in familial AD and Down's syndrome patient iPSCs, because of which patient‐specific models could be developed; these models are crucial to gain a full understanding of AD pathophysiology.67, 68, 69, 70, 71. This evidence concerns the gene MAPT and Down syndrome.