Another study further supported the role of AIM2 by suggesting that AIM2 activation by cytosolic dsDNA is responsible for the IL-1α, IFN-α, and TGF-β release from circulating monocytes of patients with prolonged COVID-19 symptoms, likely contributing to the risk of developing lung fibrosis as a sequelae (130). This evidence concerns the gene IFNA1 and COVID-19.