We found that ECs differentiated from hiPSCs (hiPSC-ECs) derived from patients with T2DM (dia-hiPSC-ECs) have signature phenotypes of ED: disrupted glycine homeostasis, ED (increased protein expression of ICAM-1 and enhanced secretion of endothelin-1), increased cell senescence, and impaired mitochondrial function [16,215]. This evidence concerns the gene EDN1 and type 2 diabetes mellitus.