To examine the potential function of MST4 in the progression of MASLD to MASH, male mice with the liver-specific depletion of MST4 and their wild-type littermates were exposed to a high-carbohydrate diet lacking methionine and choline (MCD) for 4 weeks, which mimics the main pathophysiological features of human MASH, including liver steatosis, inflammation, fibrosis, and hepatocellular injury (Figure 5A). Here, STK26 is linked to metabolic dysfunction-associated steatohepatitis.