On the other hand, within ALS subtypes linked to gain-of-function mutations of SOD1 or TARDBP (encoding TAR DNA-binding protein, TDP-43), it has been observed that mitochondrial damage caused by mutated proteins could potentially stimulate the release of mitochondrial DNA, thereby activating the cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway to potently initiate or aggravate neuroinflammation [25, 26]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.