Under hypoxia, HIF-1α can drive FTO expression, and recent work in breast cancer shows that FTO feeds a YTHDF3/PDK1–AKT–STAT3 axis to further elevate PD-L1; dual inhibition of FTO and PDK1 enhances CTL function and strengthens the effect of PD-(L)1 blockade in preclinical models. This evidence concerns the gene AKT1 and breast carcinoma.