Finally, we propose future research directions, including the tumor-specific mechanisms driving NAT10 upregulation, strategies for selectively targeting cancer <i>versus</i> normal physiology, identification of ac<sup>4</sup>C readers and erasers, and potential crosstalk between ac<sup>4</sup>C and chromatin modification, with the aim of advancing NAT10-based precision oncology. The gene discussed is NAT10; the disease is neoplasm.