HTATSF1 and breast cancer: We then confirmed in MDA-MB-231, BT-549, and T-47D cells that both HTATSF1–TOPBP1 binding and S748 phosphorylation were also controlled by CK2 kinase activity by using CK2 inhibitor treatment (Figs. 3B and S3A), and the HTATSF1–TOPBP1 association is abolished by HTATSF1/S748A mutation, whereas it is maintained by HTATSF1/S748D, which mimics pS748 (Fig. 3C and S3B), suggesting an integrity of the CK2–HTATSF1–TOPBP1 axis in breast cancer cells.