The loss or mutation of these genes significantly inhibits fatty acid metabolism, downregulating lipid content, triglyceride, and total cholesterol levels168 (Figure 4C).Recent studies have found that HIF‐1 can directly transcriptionally activate NAT10, upregulating its expression, which in turn promotes NAT10‐mediated ac4C acetylation of SEPT9 mRNA, activates the HIF‐1 pathway, regulates glucose metabolism reprogramming in gastric cancer, and forms a NAT10/SEPT9/HIF‐1 positive feedback loop, promoting glycolysis‐dependent and malignant development of gastric cancer84 (Figure 4D). The gene discussed is NAT10; the disease is gastric cancer.