[24] Increasing evidences support the idea that BBB leakage plays critical roles in AD pathogenesis.[13, 18, 25] Recently, an elegant 3D microfluidic model with human neural cell cultures was developed that could recapitulate key aspects of BBB dysfunction in AD.[15a] A hiPSC‐based 3D model has provided novel insights into pericyte ApoE4‐induced cerebral amyloid angiopathy.[13c] In this study, we demonstrated that serum exposure could induce multiple AD pathological features independently. The gene discussed is APOE; the disease is Alzheimer disease.