In the follow-up study about MA, two derivatives of MA were developed, FB23, and FB23-2, which can inhibit the LSCs of AML in vivo through inhibiting FTO and its downstream targets, such as MYC, CEBPA, RARA, and ASB2 RNA transcripts, and re-enriching m6A. This evidence concerns the gene ASB2 and acute myeloid leukemia.