Functional assays revealed that KRT8 knockdown inhibited pancreatic cancer cell proliferation and migration, whereas NAT10 knockdown and KRT8 overexpression restored these phenotypes, and overexpression of NAT10 combined with KRT8 knockdown also restored these phenotypes (Fig. 6G–L, S3A–H).These results indicate that NAT10-mediated ac4C acetylation enhances KRT8 mRNA stability and expression, thereby promoting pancreatic cancer progression. This evidence concerns the gene KRT8 and pancreatic neoplasm.