In the present study, we show that nuclear WTAP is downregulated in NASH, and hepatic deletion of Wtap leads to NASH-like phenotypes due to increased lipolysis in eWAT, increased hepatic FFAs uptake and inflammation, which are strongly associated with increased expression of Igfbp1, Cd36 and cytochemokines such as Ccl2, respectively. The gene discussed is WTAP; the disease is metabolic dysfunction-associated steatohepatitis.