Edvinas et al. [109] used retinal pigment epithelium (RPE) cells generated from Y402H (complement factor H (CFH) polymorphism Y402H)-AMD-patient-derived hiPSCs to set up an in vitro model and discovered that in Y402H-AMD-patient-specific RPE cells, the significantly increased C3 turnover led to autophagy dysfunction by increasing deposition of the terminal attack complex C5b-9 at the lysosomes, which resulted in lysosomal overburden and malfunction. The gene discussed is C3; the disease is age-related macular degeneration.