In the pathogenesis of AML-MRC-associated SS, dysregulated marrow or leukemic blasts release excessive pro-inflammatory cytokines, particularly IL-1β, IL-6, G-CSF, GM-CSF, and TNF-α, into the circulation, driving neutrophil activation, chemotaxis, and cutaneous infiltration as part of a paraneoplastic hypersensitivity reaction. This evidence concerns the gene TNF and acute myeloid leukemia.