Comparative analysis of tumor growth status revealed substantial suppression of xenograft development in PARP9 knockdown groups relative to negative controls across both CFPAC-1 and AsPC-1 models and conversely, PARP9 overexpressing PANC-1 xenografts exhibited enhanced tumorigenic potential compared to vector-control counterparts (Figures 3A–F), and knockdown or overexpression of PARP9 had no effect on body weight in mice (Supplementary Figure S6). The gene discussed is PARP9; the disease is neoplasm.