YY2 could enhance activity of the p53 promoter,[32] while suppressing that of amino‐terminal enhancer of split, thereby inhibiting tumor metastasis.[31] Furthermore, YY2 expression is aberrantly downregulated in various tumors, such as breast cancer and hepatocellular carcinoma, and its inactivation due to methylation at K279 enhances tumorigenesis.[21] Nevertheless, there is currently little knowledge regarding the mechanism responsible for the tumor suppressive effect of YY2 or its role in regulating amino acid metabolic reprogramming in tumor cells. The gene discussed is TP53; the disease is neoplasm.