23). Another substrate of PARP10 in cancer cells is the cell-cycle kinase PLK1, which is overexpressed in a variety of cancers (e.g. liver, breast and lung cancers) promoting cell proliferation and metastasis. In particular, in hepatocellular carcinoma (HCC), PARP10-mediated MARylation of PLK1 significantly inhibits its kinase activity and related oncogenic functions. Indeed, PLK1 can phosphorylate PARP10, leading to an enhanced NFκB transcriptional activity responsible for cancer progression (Ref. 24). This evidence concerns the gene PLK1 and lung carcinoma.