For instance, severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) binds to angiotensin-converting enzyme 2 and induces ROS bursts, continuously activating NF-κB, which causes alveolar epithelial cell apoptosis, increased vascular permeability, and massive infiltration of immune cells, thereby exacerbating pulmonary edema and increasing the risk of acute respiratory distress syndrome (ARDS) (Zhou et al., 2024). This evidence concerns the gene ACE2 and acute respiratory distress syndrome.