Suppression of SNORD118 and SNORD3A impairs leukemia cell proliferation and colony‐forming capacity.[33]SNORD116 and SNORD115 are highly accumulated during neuronal differentiation and are implicated in the pathogenesis of Prader‐Willi syndrome by influencing RNA stability and protein synthesis.[34] Our previous work has demonstrated that SNORD88B regulates the self‐renewal of liver cancer stem cells by anchoring WRN in the nucleolus to activate Hippo signaling.[35] However, the role of snoRNAs in ISC biology remains elusive. The gene discussed is SNORD3A; the disease is leukemia.