Our experiments showed that PMNs in ARDS could still be stimulated (by TNF/fMLP or PMA) despite high activation in ARDS but produce less ROS, which is consistent with observations available in the literature to date: PMNs from patients with severe COVID-19 disease and sepsis had a defective oxidative burst and phagocytosis despite extremely high expression of cellular and soluble activation markers (such as LOX-1) [48]. The gene discussed is FPR1; the disease is Sepsis.