For instance, in acute myeloid leukaemia, the global loss of box C/D snoRNAs with concomitant loss of ribomethylation particularly at 18S-Cm462 and 28SCm-4536(4506) is driven by MYC and the fusion oncogene AML-ETO and results in decreased self-renewal potential of leukaemic cells, while the site-specific methylation of 18S-Um116 by SNORD42A is required for leukaemia cell growth and proliferation [91,114]. This evidence concerns the gene MYC and acute myeloid leukemia.