This study explored the molecular events related to the low expression of METTL14 protein during the evolution of steatosis-MASH-liver fibrosis, including the m6A modification of GLS2 mRNA, the METTL14/GLS2/oxidative stress microenvironment signal axis, and the regulatory mechanism of macrophages and HSCs related to the progression of steatosis-MASH-hepatic fibrosis, which will help to improve the understanding of the essence of inflammatory-cancer transformation and provide theoretical and technical support for the specific prevention and treatment of MAFLD-related HCC. The gene discussed is GLS2; the disease is hepatocellular carcinoma.