We found a significant association between BRCAness and several immune-regulated signatures and evidence that several signaling pathways and processes known to modulate the immune system are activated by BRCA1 mutations or a BRCAness-related phenotype, such as JAK-STAT signaling or an interferon type I response, which are activated by free double-stranded DNA in the cytoplasm of tumor cells via the cGAS-STING pathway and affect dendritic cells (23–25). The gene discussed is SOAT1; the disease is neoplasm.