As mentioned earlier, a significant increase in proinflammatory cytokines is implicated in the pathology of COVID-19 and AS.[59,60] IL-1β, IL-6, and TNF-α are important inflammatory molecules, which induce abnormal proliferation of inflammatory cells by activating specific signaling pathways.[61] Sul and Ra[62] showed that modulating ROS, IL-1, IL-6, and TNF-α levels protected lung epithelial cells against oxidative stress and inflammation induced by lipopolysaccharide. This evidence concerns the gene IL1B and COVID-19.