In ex vivo macrophages and NK cells, treatment with subasumstat led to IFNI-dependent innate immune activation and enhanced killing of tumor cell targets (16), whereas in immunocompetent mice, subasumstat was shown to enhance antigen cross-presentation and promote T- and NK-cell activation through increases in CD69 and CD80/CD86 surface proteins, respectively (15, 18). Here, CD69 is linked to neoplasm.