As self-DNA (nuclear and/or mitochondrial) has been shown to stimulate STING in autoinflammatory and malignant disease (47–50), and both AML growth and chemotherapy-induced DNA damage dysregulate the BM apoptotic response (51, 52), we hypothesized that AML-specific BMM STING activation is mediated by local tumor cell apoptosis and cellular debris. The gene discussed is STING1; the disease is acute myeloid leukemia.