In nonalcoholic fatty liver disease, endogenous denatured DNA, cholesterol, and HMGB1 derived from apoptotic and necrotic host cells, together with mtDNA, formylated peptides, and ATP released due to mitochondrial dysfunction, induce inflammation by activating the cGAS/STING pathway and NLRP3 inflammasomes [267]. The gene discussed is STING1; the disease is metabolic dysfunction-associated steatotic liver disease.