NOX4OE CB-ECFCs also showed reduced p53 phosphorylation (S46), with network analysis revealing linkage to downstream positive regulation of endoglin and E2F1 expression, indicating that NOX4-mediated inhibition of p53 activation may heighten ECFC resilience to hyperglycaemia-mediated and p53-dependent cell cycle arrest, apoptosis and senescence [31–33]. The gene discussed is NOX4; the disease is Hyperglycemia.