According to previous literature reports (Zhang et al., 2016; Adameova et al., 2022), CaMKII triggers the opening of the mitochondrial permeability transition pore and myocardial necroptosis through phosphorylation, oxidation, or both, CaMKII inhibition has been shown to alleviate oxidative stress and apoptosis by restoring IRE1α/XBP1s signaling (Kong et al., 2022), yet its role in modulating the redox reactions in ARDS has not been previously documented. The gene discussed is CAMK2G; the disease is acute respiratory distress syndrome.