In conclusion, we provided compelling in vitro and in vivo evidence revealing an oncogenic role of NAT10 in CCa progression and determined that as an essential epitranscriptomic regulator, NAT10‐mediated ac4C modification in tumor cells upregulates the TF FOXP1, which increases Treg infiltration and promotes CCa immunosuppression by reprogramming glycolytic metabolism. The gene discussed is TF; the disease is neoplasm.