The mitochondrial deacetylase SIRT3 regulates ROS levels, thereby affecting HIF-1α stability and overall metabolic reprogramming.245 Similarly, SIRT4 contributes through its impact on ROS-mediated HIF-1α stabilization.246 Additionally, mitochondrial UQCC3 maintains HIF-1α stability by modulating ROS production, thereby influencing cancer cell metabolic adaptation.247 These complex interactions underscore the critical role of mitochondrial function in regulating HIF-mediated responses. This evidence concerns the gene HIF1A and cancer.