We thus examined the involvement of PARP4’s ADP-ribosylation catalytic activity in its tumor suppressive function by overexpressing mutant PARP4 lacking its PARP catalytic domain in PARP4 clonal knockout iSAEC-K cells, which were used in subsequent in vivo tumorigenicity assays (Additional file 1: Figure S3G, H). This evidence concerns the gene PARP4 and neoplasm.