For instance, SNORA13 directly interacted with RPL23 to regulate the p53 pathway.[38]SNORD50A and SNORD50B inhibited cancer progression by directly binding with K‐Ras and contributed to its degradation.[39] We just reported that a C/D box snoRNA SNORD88B drives self‐renewal of liver CSCs through anchoring WRN in the nucleolus in a non‐canonical mechanism.[19] Up to date, however, there is no report on involvement of H/ACA box snoRNA‐mediated non‐canonical mechanism in the regulation of CSCs. The gene discussed is KRAS; the disease is cancer.