TBK1 and neoplasm: Consequently, using the phosphorylation of TBK1 as a functional marker to monitor the activities of innate immune signals in tumor cells, we found that the PRMTi treatment alone induced comparable levels of p-TBK1 as the PARPi treatment, whereas the combination of PRMTi and PARPi increased p-TBK1 remarkably compared with single agent treatments (Figure S5E).