Here we show that developing resistant phenotypes during tyrosine kinase inhibitor (TKI) therapy depends on m<sup>6</sup>A reduction resulting from FTO overexpression in leukemia cells.
The identification of radicicol as an FTO inhibitor and revelation of its recognition mechanism not only opens the possibility of developing new therapeutic strategies for treatment of leukemia but also provide clues for elucidation of the acting mechanisms of radicicol, which is a possible clinical candidate worth in-depth study.
As the first identified messenger RNA <i>N</i><sup>6</sup>-methyladenosine (m<sup>6</sup>A) demethylase, FTO has been shown recently to play m<sup>6</sup>A-dependent roles in adipogenesis and tumorigenesis (especially in the development of leukemia and glioblastoma).