More recently, iPSC-ECs generated from patients with familial hypercholesterolemia (FH) due to LDLR mutations were found to display reduced LDL uptake, impaired angiogenic capacity, and heightened inflammatory and oxidative stress signatures, providing a platform to interrogate endothelial susceptibility to atherosclerosis and to test lipid-lowering or anti-inflammatory interventions in a patient-specific manner. Here, LDLR is linked to familial hyperaldosteronism.