This highlights the metabolic plasticity of deacetylases such as SIRT6, which can function as oncogenes or tumor suppressors depending on the tumor microenvironment.49 This duality is paralleled by ACAT2, in which our results revealed that ACAT2 has a protumorigenic role, which is different from previous studies that associated low ACAT2 expression with poor survival in patients with ccRCC.52 These discrepancies may stem from differences in tumor stage or molecular context, as cholesterol esterification by ACAT2 confers a survival advantage, especially in lipid-rich tumors. The gene discussed is ACAT2; the disease is neoplasm.