A consistent theme across models is that hypoxia-driven programs remodel m6A dynamics: HIF-1α can transcriptionally induce the demethylase FTO, which elevates PD-L1 via a PDK1–AKT–STAT3 cascade and blunts T-cell attack; pharmacologic or genetic reduction of FTO in hypoxia restores sensitivity to PD-L1 blockade in preclinical breast cancer, directly linking a stress sensor to immune resistance. The gene discussed is AKT1; the disease is breast cancer.