FTO is an RNA N6-methyladenosine (m6A) demethylase that regulates fat mass, adipogenesis, and energy homeostasis. It catalyzes oxidative demethylation of mRNAs, tRNAs, and snRNAs, with m6A being the most prevalent internal mRNA modification in eukaryotes. By removing m6A marks from target transcripts, FTO modulates mRNA expression and stability, influencing cellular processes including adipogenic differentiation and brown fat thermogenesis. FTO expression is dysregulated across multiple disease contexts. In acute myeloid leukemia, FTO promotes oncogenic transformation by demethylating m6A in MYC, CEBPA, ASB2, and RARA transcripts 1. In pancreatic cancer, FTO enhances gemcitabine resistance through m6A-dependent regulation of NEDD4 mRNA stability and the PTEN/PI3K/AKT pathway 2. FTO is also implicated in cardiovascular pathology, with genetic variants associated with hypertension and atherosclerosis progression 3, and in systemic lupus erythematosus where elevated FTO expression drives autoimmune B-cell expansion via the TLR7-m6A-ATP6V1G1 axis 4. Small-molecule FTO inhibitors including FB23-2 and meclofenamic acid have shown promise in preclinical AML models, suppressing leukemic cell proliferation and promoting differentiation 15. These findings establish FTO as a druggable target across oncologic and metabolic disease contexts.