In preclinical studies, inhibition of SIRPα signaling in CD8α+ type I conventional dendritic cells has been shown to enhance sensing of phagocytosed tumor mitochondrial DNA, which triggers the cGAS/STING-mediated type I interferon response that facilitates cross-presentation of tumor antigens to CD8 T cells (6, 7). The gene discussed is CGAS; the disease is neoplasm.