In parallel, proteomic profiling of CRISPR/Cas9-generated MST3 knockout and wild-type Huh7 cells was conducted to gain molecular insight into MST3-regulated pathways.<h4>Results</h4>Mst3 ASO therapy had no impact on the onset or aggravation of experimentally induced MASH-associated HCC in mice, despite markedly improving the whole-body metabolic profile and suppressing all key features of MASH. The gene discussed is STK24; the disease is hepatocellular carcinoma.