For example, CD133 can recruit HDAC6 to deacetylate β‐catenin to activate β‐catenin signaling.[15] Our previous studies have shown that the interaction between CD133 and the PI3K regulatory subunit p85 can activate the PI3K/Akt pathway to promote tumorigenesis of GSCs.[16] In addition, activation of FAK by the interaction between CD133 and Src promoted the migration of tumor cells.[17] Collectively, CD133 is a functional marker of CSCs. The gene discussed is PROM1; the disease is neoplasm.