Noncanonical STING/PERK/eukaryotic initiation factor 2α (eIF2α) signaling drives pulmonary and renal fibrosis, and is a potential therapeutic target.[464, 465] The activation of cGAS/STING signaling promotes hepatic fibrosis and the development of hepatic sinusoidal microthrombosis.[466] Oxidative stress‐mediated ferroptosis in hepatocytes regulates STING activation in macrophages, leading to hepatic injury and fibrosis.[467]. This evidence concerns the gene STING1 and Hepatic fibrosis.