An antisense oligonucleotide (ASO) that switches PKM splicing from tumor-promoting PKM2 to the PKM1 isoform limits aerobic glycolysis, thereby inhibiting HCC growth both in vitro and in vivo, laying the groundwork for a potential ASO-based splicing therapy in treating liver cancer [105,106]. The gene discussed is PKM; the disease is hepatocellular carcinoma.