In a metabolic dysfunction-associated steatohepatitis (MASH) model of advanced liver fibrosis, antisense oligonucleotides (ASOs) against Hic-5 significantly reduced α-SMA expression and collagen deposition, leading to attenuated fibrosis and even improvement of liver steatosis [4]. Here, ACTA1 is linked to metabolic dysfunction-associated steatohepatitis.