TNF and acute myeloid leukemia: LSCs produce TNF‐α, and this upregulates the NF‐κB pathway in an autocrine manner, worsening disease progression in AML and CML.(92, 93) Furthermore, leukemic cells can polarize macrophages to a leukemia‐supportive phenotype through growth factor independence 1 (Gfi1),(94) a transcription factor necessary for the regulation of normal hematopoiesis that has been previously linked to leukemic development.(95, 96)