Decreased nuclear WTAP in NASH leads to the impairment of the WTAP/HDAC1 axis and increases the transcription of Igfbp1, Cd36 and Ccl2, which further increases lipolysis in WAT, hepatic FFA uptake and liver inflammation, respectively, finally causing NASH pathogenesis. The gene discussed is HDAC1; the disease is metabolic dysfunction-associated steatohepatitis.