SLC16A3 and neoplasm: ALKBH5 tunes the lactate efflux program (via MCT4/SLC16A3), increasing local acidosis and favoring the accumulation of Tregs and MDSCs; genetic deletion or small-molecule inhibition of ALKBH5 reduces these suppressive infiltrates and improves anti-PD-1 efficacy in multiple syngeneic models, directly tying an m6A eraser to the composition of tumor-infiltrating immune cells.