Inhibition of BACH1 is able to suppress tumor‐initiating CSC markers (OCT4, SOX2, NANOG, and CD44), tumor‐sphere formation, and CSC growth and metastasis in the xenograft model of mice.[162] BACH1 mediated the upregulation of mitochondrial ROS and CSC‐marker expression stimulated by chronic intermittent hypoxia.[163] Accordingly, BACH1 also elevates the mRNA levels of stemness‐associated genes (including CD133, and CD44), and contributes to maintaining the cancer stemness of hepatocellular carcinoma cells. The gene discussed is PROM1; the disease is cancer.