The m⁶A epitranscriptomic landscape in T-ALL and therapeutic implications of targeting HNRNPC and FTO. m⁶A is regulated by “writers” (METTL3/14, WTAP, VIRMA, RBM15, HAKAI) and “erasers” (FTO, ALKBH5). In T-ALL, global m⁶A is reduced, but MYC and cholesterol-related transcripts are hypermethylated and recognized by HNRNPC, enhancing their translation and promoting leukemia. METTL3 inhibition paradoxically increases m⁶A and expression of MYC and cholesterol metabolism despite reduced global m⁶A. In contrast, FTO inhibition lowers MYC and metabolic gene expression. FTO inhibition or HNRNPC loss impairs cholesterol metabolism, reduces MYC, and decreases leukemic proliferation and survival, ultimately lowering T-ALL burden.