The current treatment strategy of NASH in clinical settings is, unfortunately, limited to farnesoid X receptor (FXR) agonists (e.g., obeticholic acid) and some antidiabetic drugs (e.g., thiazolidinediones), which prove inadequate in hepatoprotection and arresting progression to more severe hepatic dysfunctions such as hepatic fibrosis [4, 5]. Here, NR1H4 is linked to metabolic dysfunction-associated steatohepatitis.