Whilst others have reported similar decreases in ECFC function [15, 16, 23] and implicated NOX4 as a pivotal regulator of altered EC homeostasis in diabetes [45, 46], here we present novel data indicating that reduced angiogenic capacity and eNOS activation, which is regulated by NOX4 [47], is associated with markedly decreased NOX4 protein expression in CB-ECFCs exposed to hyperglycaemia. The gene discussed is NOS3; the disease is diabetes mellitus.