Defects in m6A methylation affect diverse biological processes, including cancer initiation, development and progression.(31–35) We recently demonstrated that a dynamic FTO/m6A axis emerges as a key epigenetic driver of reversible TKI-tolerance state making contribution to acquired TKI resistance through activating cell proliferation/anti-apoptotic genes.(36) Yet, it is not well understood whether and how the FTO/m6A axis empowers leukemia cells to survive prolonged drug exposure through non-protein coding genes. This evidence concerns the gene FTO and cancer.