The compounds selectively inhibited the demethylation of FTO in AML cells, upregulated the m6A modification on the mRNA of key AML genes, increased the abundance of oncogenic proteins such as ASB2 and RARA, and decreased the abundance of oncogenic proteins such as MYC and CEBPA, thereby inhibiting the proliferation of AML cells, and demonstrated the anti-leukemia therapeutic effect in a PDX mouse model. The gene discussed is MYC; the disease is leukemia.