Given the interest in translesion synthesis (TLS) polymerases as therapeutic targets in cancer [31–33] and our observation that all the HORMAD1 expressing breast cancer cell lines showed sensitivity to POLH knockdown (Fig. S7), we further investigated how the silencing of POLH and a wider group of TLS polymerases, affected the viability of HORMAD1-expressing cells. The gene discussed is HORMAD1; the disease is breast cancer.