Notably, the cytokines (tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), IL-6, IL-8, IL-12, and IL-17, macrophage inflammatory protein (MIP-1), vascular endothelial growth factor (VEGF)), chemokines (CXCL1 and CXCL8), ROS, and metalloproteinases 1 and 9 (MMP-1 and MMP-9) triggered in the acute phase of COVID-19 can promote alveolar destruction and tissue remodeling, leading to pulmonary fibrosis [2,10,11,12]. Here, IL17A is linked to COVID-19.