NAT10 and cancer: As shown in Fig. 2C-G and Additional file 1: Fig. S2C, S3E-F, re-expression of wild-type NAT10 in NAT10-knockout cells effectively rescued ac4C acetylation and corresponding changes to cancer cell physiology, whereas neither of the two NAT10 mutants exhibited these effects, suggesting that the RNA ac4C modification function of NAT10 is indispensable for its role in promoting gastric carcinogenesis.