TNFRSF11A and acute myeloid leukemia: The remaining eight molecular systems components (arginase signaling, CCL2 signaling, PD-L1 signaling, IDO signaling, Tim-3 signaling, TLR-2 signaling, the AHR pathway, and RANK/RANKL signaling) contribute to AML pathogenesis by promoting immune evasion and suppression.