Our recent report demonstrated that in diet‐induced obese mice, myeloid GHSR deletion protects against hepatic steatosis and inflammation through protein kinase A (PKA)−cyclic adenosine monophosphate responsive element binding protein (CREB)−insulin receptor substrate 2 (IRS2) (PKA−CREB−IRS2) signaling cascade.[15] In the present study, we used the chronic CCl4 treatment model to investigate the role of macrophage GHSR in liver fibrosis. Here, GHSR is linked to fatty liver disease.