Convergently across disease sites, near-term opportunities include: pairing FTO or ALKBH5 inhibitors with RT to broaden the therapeutic window; testing reader antagonism (YTHDF1/2) to preserve RT-elicited STING–IFN and cross-priming, combining METTL3 inhibition with venetoclax or cytotoxics in AML; and deploying NAT10 inhibitors where ac4C programs drive resistance or immune suppression (melanoma, TNBC). The gene discussed is STING1; the disease is acute myeloid leukemia.