Moreover, thioredoxin promoted the stemness of hepatocellular carcinoma cells by interacting with BACH1, stabilizing BACH1 expression by inhibiting its ubiquitination, and facilitated hepatocellular carcinoma metastasis both in vitro and in vivo.[164] Thus, BACH1 may act as a central hub, bringing together NANOG, SOX2, and OCT4 to stabilize these factors, and meanwhile, it increases the transcription of CD44 and CD133, ultimately contributing to the enhancement of cancer stem cell‐like properties. This evidence concerns the gene CD44 and hepatocellular carcinoma.