Several recent studies have documented the essential role of GAS5 as a “molecular switch” to control quiescence/stemness in CSCs, including the CD133 + CSCs in pancreatic cancer [43] and HCT116-derived CSCs [44], as well as for self-renewal and pluripotency of mouse embryonic stem cells [45]. The gene discussed is PROM1; the disease is pancreatic neoplasm.