SOX2 has been shown to mediate metabolic reprogramming in cancer cells by enhancing glycolysis.[30, 31, 32] To examined whether elevated SOX2 accounted for dysregulation of mitochondrial function, we first analyzed SOX2 binding sites using published ChIP‐seq data from human iPSCs[33] and obtained 3741 peaks after filtering out peaks with enrichment scores under 25. The gene discussed is SOX2; the disease is cancer.