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. Here, PROM1 is linked to hepatocellular carcinoma.