Activation of a NOX4-Nrf2-HO-1 axis triggered by dietary-derived TRLs in vivo may, therefore, be fundamentally important for adaptive protection of the vessel wall in the postprandial phase and for mitigating the postprandial inflammation thought to encourage development of endothelial dysfunction and its detrimental consequences (3). The gene discussed is NOX4; the disease is endothelial dysfunction.