The relationship between genomic instability and immune responses in TNBC, through HORMAD1 Triple-negative breast cancers are characterised by extensive inter- and intra-tumoural heterogeneity, encompass clinically and biologically distinct subgroups, display a diverse landscape of immune cell infiltrates, and are driven by a spectrum of genomic alterations. This complexity provides a real challenge for patient management. As part of the Breast Cancer Now Research Unit at King’s, we identified HORMAD1, a Cancer/Testis antigen, as a driver of genomic instability in TNBC. Cancer/Testis antigens are well-known for their immunogenic capabilities and a relatively small subset of these antigens also play an essential role in meiomitosis. We study the molecular mechanisms by which HORMAD1 causes genomic instability, leading to innate and adaptive immune responses and in doing so, ultimately inform the design of therapeutic approaches for a subgroup of HORMAD1-expressing Triple-negative breast cancers.