Critically, we showed that a Snord67 construct with a point mutation in the antisense element fails to rescue U6 C60 methylation and only partially rescues in vitro colony formation and spheroid area in Snord67 knockout cells (Fig. 2), suggesting that the canonical function of Snord67 in guiding U6 C60 methylation is important for its role in promoting tumor growth. The gene discussed is SNORD67; the disease is neoplasm.