For example, Myc has been demonstrated to promote acetylation‐dependent inactivation of SDHA by activating SKP2‐mediated degradation of the SIRT3 deacetylase, reducing SDH activity and causing cellular succinate accumulation, which triggers H3K4me3 activation and tumor‐specific gene expression.[29] Furthermore, SDHA is the only known acetylated subunit in complex II, and SDH activity correlates with the acetylation level of SDHA.[28] During reperfusion, the oxidation of succinate, which accumulates in large amounts during ischemia, is a major contributor to I/R injury. This evidence concerns the gene SDHA and neoplasm.