Consequently, B7‐H4 undermines the cascade of events that would typically lead to the release of DAMPs associated with immunogenic cell death (ICD), preventing the phagocytosis of tumor cells by dendritic cells and ultimately obstructing T cell recruitment to the tumor site.[3] In this regard, the elevated B7‐H4 expression may pose a significant barrier for a subgroup of TNBC patients receiving SG treatment which was also validated in this study, where TNBC cells with high B7‐H4 exhibited significantly lower response to SG treatment. The gene discussed is VTCN1; the disease is neoplasm.