Our study also evaluated the therapeutic potential of targeting N1DARP using a modified stapled peptide derived from N1DARP, SAH-mAH2-5, which perturbs the USP10–N1ICD interaction and suppresses tumor growth in Notch1-activated pancreatic cancer, thus providing insights into how the N1DARP–N1ICD interaction could be targeted for the development of precise and individualized pancreatic cancer therapy. This evidence concerns the gene USP10 and pancreatic neoplasm.