To conclude, several patterns are consistent across teams: (i) NK cells require intact m6A writer/reader activity for antitumor function; (ii) DC YTHDF1 restrains cross-priming, so its inhibition can be immunostimulatory; (iii) in myeloid cells, reducing ADAR1 or recalibrating m6A often shifts toward pro-inflammatory, T-cell-permissive states; and (iv) Treg-specific loss of YTHDF2 diminishes suppression and improves tumor control (53, 88, 93). The gene discussed is YTHDF1; the disease is neoplasm.