IRF3 and Hepatic fibrosis: Iracheta-Vellve, A. et al. demonstrated that in CCL4-treated hepatocytes, endoplasmic reticulum (ER) stress via STING triggered TBK1 phosphorylation, followed by IRF3 phosphorylation, which then interacted with BAX in mitochondria through its BH3-only structural domain, leading to pro-apoptotic caspase 3 activation and hepatocyte apoptosis, ultimately contributing to liver fibrosis [98].