Moreover, the etiopathology of lung inflammation in patients with silicosis is associated with a significant increase in the release of chromatin fragments and mtDNA from dying cells into the bronchoalveolar lavage fluid (BALF) after silica exposure, inducing excess production of type-I IFN and CXCL10 via cGAS–STING activation [171]. Here, STING1 is linked to silicosis.