Myeloid-specific STING induced TGF-β1 and activated hepatic stellate cells (HSCs), which promoted NASH progression, whereas disruption of myeloid STING alleviated hepatic inflammation, steatosis, and liver fibrosis in a mouse model of HFD or methionine and choline-deficient diet (MCD)-induced NASH (72), suggesting that activation of STING regulates macrophage function and augments hepatic lipid accumulation, profibrotic gene expression, and proinflammatory responses in NASH (Figure 2). Here, STING1 is linked to metabolic dysfunction-associated steatohepatitis.